tag:blogger.com,1999:blog-64073593629297395342024-03-04T21:35:44.172-08:00Apigenin Research News - ScienceCurrent apigenin research results and its effects on autophagy, cancer, apoptosis, antiaging and allergyAnonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.comBlogger13125tag:blogger.com,1999:blog-6407359362929739534.post-33516287910077495372014-11-21T03:42:00.000-08:002014-11-21T03:42:03.212-08:00Apigenin can protect cardiomyocytes<h3>
Protective Effect of Apigenin on Ischemia/Reperfusion Injury of the Isolated Rat<br />Heart.</h3>
<a href="http://apigeninresearch.blogspot.com/">Apigenin</a> can protect cardiomyocytes from I-/R-induced injury, at least partially, through the inhibition of p38 MAPKS signaling pathway.<br />
<br />
Cardiovasc Toxicol. 2014 Nov 7. [Epub ahead of print]<br />
<br />
Hu J(1), Li Z, Xu LT, Sun AJ, Fu XY, Zhang L, Jing LL, Lu AD, Dong YF, Jia ZP.<br />
<br />
<a name='more'></a><br />
<br />
Author information:<br />
<br />
(1)Department of Pharmacy, General Hospital of Lanzhou Command, PLA, Lanzhou,<br />
730050, China, hujinglzbx@163.com.<br />
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Apigenin (Api), a mainly bioactive component of Apium graveolens L. var. dulce<br />
DC. (a traditional Chinese medicinal herb), possesses a wide range of biological<br />
activities, including antioxidant effects. It also has been shown to associate<br />
with lower prevalence of cardiovascular diseases, but its mechanisms of action<br />
remain unclear. The aim of the present study is to investigate the role of Api in<br />
isolated rat heart model of ischemia/reperfusion (I/R). Langendorff-perfused<br />
isolated rat hearts were used in our study. Api was added to the perfusate before<br />
ischemia and during reperfusion in the isolated pulsed rat heart exposed to<br />
30-min ischemia followed by 50-min reperfusion. The treatment with Api conferred<br />
a cardioprotective effect, and the treated hearts demonstrated an improved<br />
ischemic cardiac functional recovery, a decreased myocardial infarct size, a<br />
reduced activities of creatine kinase isoenzyme and lactate dehydrogenase in the<br />
coronary flow, a reduced number of apoptotic cardiomyocytes, a reduced activity<br />
of caspase-3, up-regulation of the anti-apoptotic protein <a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">Bcl-2</a> and<br />
down-regulation of the pro-apoptotic protein Bax. In addition, Api inhibited the<br />
phosphorylation of p38 MAPKS during I/R. In conclusion, these observations<br />
provide preliminary evidence that Api can protect cardiomyocytes from<br />
I-/R-induced injury, at least partially, through the inhibition of p38 MAPKS<br />
signaling pathway.<br />
<br />
Hu J, Li Z, Xu LT, Sun AJ, Fu XY, Zhang L, Jing LL, Lu AD, Dong YF, Jia ZP.<br />
Protective Effect of Apigenin on Ischemia/Reperfusion Injury of the Isolated Rat<br />
Heart. Cardiovasc Toxicol. 2014 Nov 7. [Epub ahead of print] PubMed PMID:<br />
25377428.Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-4375734362309271192014-11-17T13:28:00.000-08:002014-11-17T13:28:38.417-08:00Berberine induces apoptosis<pre><div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhThxRMssKGh9GXengFMKAvbwIk7ZL-cM4WW_emXeamu4ep3swHnA-AF_6QXirzxjMAjS-meTx68q3a2nJ8SYpCqM_3E4cyXxuuYeUT9N3GMtuWWgUabcUt91GiLPC3KJlCld4eXAQP9Hk/s1600/berberine+and+apoptosis.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="berberine kills cancer cells" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhThxRMssKGh9GXengFMKAvbwIk7ZL-cM4WW_emXeamu4ep3swHnA-AF_6QXirzxjMAjS-meTx68q3a2nJ8SYpCqM_3E4cyXxuuYeUT9N3GMtuWWgUabcUt91GiLPC3KJlCld4eXAQP9Hk/s1600/berberine+and+apoptosis.jpg" height="195" title="berberine induces apoptosis" width="200" /></a></div>
<h3>
<span style="color: blue; font-family: Arial, Helvetica, sans-serif;">Berberine affects human cancer cells</span></h3>
<span style="font-family: Arial, Helvetica, sans-serif;">
</span>
<span style="font-family: Arial, Helvetica, sans-serif;">1. Mol Med Rep. 2014 Dec;10(6):3132-8. doi: 10.3892/mmr.2014.2608. Epub 2014 Oct 8.</span>
<h3>
<span style="font-family: Arial, Helvetica, sans-serif;">Berberine sensitizes rapamycin‑mediated human hepatoma cell death in vitro.</span></h3>
<span style="font-family: Arial, Helvetica, sans-serif;">Guo N(1), Yan A(1), Gao X(1), Chen Y(2), He X(1), Hu Z(1), Mi M(1), Tang X(3),
Gou X(1).</span>
<span style="font-family: Arial, Helvetica, sans-serif;">
<i>Author information: </i></span>
<span style="font-family: Arial, Helvetica, sans-serif;"><i>
(1)Laboratory of Cell Biology and Translational Medicine, Institute of Basic Medical
Science, X'ian Medical University, Xi'an, Shaanxi 710021, P.R. China.
(2)Department of Cell Biology and Genetics, College of Medicine, Xi'an Jiaotong
University, Xi'an, Shaanxi 710032, P.R. China.
(3)Department of Pathology, Sichuan College of Traditional Chinese Medicine,
Mianyang, Sichuan 721000, P.R. China.</i></span>
<span style="font-family: Arial, Helvetica, sans-serif;">
Rapamycin is clinically used as an immunosuppressant. Increasing evidence suggests that rapamycin has an important inhibitory role in the development and progression of different types of cancer and that it is a promising candidate for cancer chemotherapy. Berberine is an isoquinoline alkaloid isolated from medicinal plant species, which has been used in traditional Chinese medicine with no significant side effects. Recent research has demonstrated that berberine has anticancer activity against various types of cancer, mediated through the suppression of <a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">mammalian target of rapamycin (mTOR)</a>. The present study aimed to investigate the in vitro synergistic anticancer effect of combined treatment of rapamycin at various concentrations (0, 10, 50, 100 and 200 nM) and berberine (62.5 µM) in SMMC7721 and HepG2 hepatocellular carcinoma (HCC) cell lines, and the potential underlying molecular mechanism. The combined use of rapamycin and berberine was found to have a synergistic cytotoxic effect, with berberine observed to maintain the cyotoxic effect of rapamycin on HCC cells at a lower rapamycin concentration. </span><span style="font-family: Arial, Helvetica, sans-serif;">Moreover, the cells treated with the combination of the two agents exhibited significantly decreased protein levels of phosphorylated (p)‑p70S6 kinase 1 (Thr389), the downstream effector of mTOR, compared with the cells treated with rapamycin or berberine alone. Furthermore, overexpression of cluster of differentiation (CD) 147, a transmembrance glycoprotein associated with the anticancer effects of berberine, was found to upregulate p‑mTOR expression and inhibit cell death in SMMC7721 cells co‑treated with rapamycin and berberine. In conclusion, the findings of the present study suggest that the combined use of rapamycin and berberine may improve HCC therapy through synergistically inhibiting the mTOR signaling pathway, which is at least in part, mediated through CD147.<a name='more'></a></span></pre>
<pre><span style="font-family: Arial, Helvetica, sans-serif;">
</span></pre>
<pre><span style="font-family: Arial, Helvetica, sans-serif;">
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2. Mol Med Rep. 2014 Nov 12. doi: 10.3892/mmr.2014.2929. [Epub ahead of print]
</span>
<h3>
<span style="font-family: Arial, Helvetica, sans-serif;">Berberine targets epidermal growth factor receptor signaling to suppress prostate </span><span style="font-family: Arial, Helvetica, sans-serif;">cancer proliferation in vitro.</span></h3>
<span style="font-family: Arial, Helvetica, sans-serif;"><i>Huang ZH, Zheng HF, Wang WL, Wang Y, Zhong LF, Wu JL, Li QX.</i></span>
<span style="font-family: Arial, Helvetica, sans-serif;"><i>
Author information:
Department of Urological Surgery, Kunshan First People's Hospital Affiliated to
Jiangsu University, Kunshan, Jiangsu 215300, P.R. China.</i></span>
<span style="font-family: Arial, Helvetica, sans-serif;">
Berberine is a well‑known component of the Chinese <a href="http://apigeninresearch.blogspot.com/">herbal medicine</a> Huanglian
(Coptis chinensis), and is capable of inhibiting the proliferation of multiple
cancer cell lines. However, information available regarding the effect of
berberine on prostate cancer cell growth is limited. In the present study, LnCaP
and PC‑3 human prostate cancer cell lines were selected as in vitro models in
order to assess the efficacy of berberine as an anticancer agent. A cell
proliferation assay demonstrated that berberine inhibited cell growth in a
dose‑and time‑dependent manner. Further investigation revealed berberine
significantly accumulated inside cells that were in the G1 phase of the cell
cycle and enhanced apoptosis. Western blot analysis demonstrated that berberine
inhibited the expression of prostate‑specific antigen and the activation of
epidermal growth factor receptor (EGFR), and it attenuated EGFR activation
following EGF treatment in vitro. In conclusion, the results indicate that
berberine inhibits the proliferation of prostate cancer cells through apoptosis
and/or cell cycle arrest by inactivation of the EGFR signaling pathway.
PMID: 25394789 [PubMed - as supplied by publisher]
</span>
<span style="font-family: Arial, Helvetica, sans-serif;">
</span>
<span style="font-family: Arial, Helvetica, sans-serif;">3. Mini Rev Med Chem. 2014 Nov 7. [Epub ahead of print]
</span>
<h3>
<span style="font-family: Arial, Helvetica, sans-serif;">Alpha-Helical Cationic Anticancer Peptides: A Promising Candidate of Novel Anticancer Drugs.</span></h3>
<span style="font-family: Arial, Helvetica, sans-serif;"><i>Huang Y, Feng QI, Yan Q, Hao X, Chen Y(1).</i></span>
<span style="font-family: Arial, Helvetica, sans-serif;"><i>
Author information: </i></span>
<span style="font-family: Arial, Helvetica, sans-serif;"><i>
(1)College of Life Sciences, Jilin University, Changchun, China.
chen_yuxin@jlu.edu.cn.</i></span>
<span style="font-family: Arial, Helvetica, sans-serif;">
<a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">Cancer</a> has become a great concern in public health. The harmful side effects and
multidrug resistance of traditional chemotherapy prompt urgent needs for novel
anticancer drugs or therapeutic approaches. Anticancer peptides (ACPs) have
become promising molecules as new anticancer agents due to the unique mechanism
and several extraordinary properties. Most α-helical ACPs target on cell membrane
and the interactions between ACPs and cell membrane components are believed to be
a key factor in the selective killing of cancer cells. In this review, we focus
on the exploitation of the structure and function of α-helical ACPs, including
the distinction of cancer cells and normal cells, the proposed anticancer
mechanisms, and the influence of physicochemical parameters of α-helical ACPs on
the biological activities and selectivity against cancer cells. In addition, the
design and modification methods to optimize the cell selectivity of α-helical
ACPs are also considered. Finally, the suitability of ACPs as cancer therapeutics
is also discussed.</span>
<span style="font-family: Arial, Helvetica, sans-serif;">
4. Eur J Pharmacol. 2014 Oct 5;740:584-95. doi: 10.1016/j.ejphar.2014.06.025. Epub
2014 Jun 26.
</span>
<h3>
<span style="font-family: Arial, Helvetica, sans-serif;">Targets and mechanisms of berberine, a natural drug with potential to treat cancer with special focus on breast cancer.</span></h3>
<span style="font-family: Arial, Helvetica, sans-serif;"><i>Jabbarzadeh Kaboli P(1), Rahmat A(2), Ismail P(3), Ling KH(4).</i></span>
<span style="font-family: Arial, Helvetica, sans-serif;"><i>
Author information: </i></span>
<span style="font-family: Arial, Helvetica, sans-serif;">
<i>(1)Department of Biomedical Science, Faculty of Medicine and Health Sciences,
Universiti Putra Malaysia, UPM Serdang 43400, Selangor, Malaysia; Department of
Nutrition and Dietetics, Faculty of Medicine and Health Sciences, Universiti
Putra Malaysia, UPM Serdang 43400, Selangor, Malaysia. Electronic address:
pjabbarzadeh@gmail.com.
(2)Department of Nutrition and Dietetics, Faculty of Medicine and Health Sciences,
Universiti Putra Malaysia, UPM Serdang 43400, Selangor, Malaysia. Electronic
address: asmah@upm.edu.my.
(3)Department of Biomedical Science, Faculty of Medicine and Health Sciences,
Universiti Putra Malaysia, UPM Serdang 43400, Selangor, Malaysia. Electronic
address: patimah@upm.edu.my.</i></span>
<span style="font-family: Arial, Helvetica, sans-serif;"><i>(4)Department of Obstetrics and Gynecology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, UPM Serdang 43400, Selangor, Malaysia; Genetics and
Regenerative Medicine Research Centre, Faculty of Medicine and Health Sciences,
Universiti Putra Malaysia, UPM Serdang 43400, Selangor, Malaysia.</i></span>
<span style="font-family: Arial, Helvetica, sans-serif;">
<a href="http://apigeninresearch.blogspot.com/2014/11/apigenin-and-breast-cancer.html">Breast cancer</a> is the most common cancer among women worldwide and novel
therapeutic agents are needed to treat this disease. The plant-based alkaloid
berberine has potential therapeutic applications for breast cancer, although a
better understanding of the genes and cellular pathways regulated by this
compound is needed to define the mechanism of its action in cancer treatment. In
this review, the molecular targets of berberine in various cancers, particularly
breast cancer, are discussed. Berberine was shown to be effective in inhibiting
cell proliferation and promoting apoptosis in various cancerous cells. Some
signaling pathways affected by berberine, including the MAP (mitogen-activated
protein) kinase and Wnt/β-catenin pathways, are critical for reducing cellular
migration and sensitivity to various growth factors. This review will discuss
recent studies and consider the application of new prospective approaches based
on microRNAs and other crucial regulators for use in future studies to define the
action of berberine in cancer. The effects of berberine on cancer cell survival
and proliferation are also outlined.</span>
<span style="font-family: Arial, Helvetica, sans-serif;">
5. Mol Med Rep. 2014 Oct;10(4):1734-8. doi: 10.3892/mmr.2014.2405.
</span>
<h3>
<span style="font-family: Arial, Helvetica, sans-serif;">Berberine induces apoptosis and DNA damage in MG‑63 human osteosarcoma cells.</span></h3>
<span style="font-family: Arial, Helvetica, sans-serif;"><i>Zhu Y(1), Ma N(2), Li HX(3), Tian L(4), Ba YF(5), Hao B(6).
Author information:
(1)Department of Orthopedic Surgery, The Second Affiliated Hospital of Zhengzhou
University, Zhengzhou, Henan 450014, P.R. China.
(2)Department of Interventional Radiology, The First Affiliated Hospital of
Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
(3)Department of Pathology, The First Affiliated Hospital of Zhengzhou University,
Zhengzhou, Henan 450052, P.R. China.
(4)Department of Medicine, Zhengzhou Ninth People's Hospital, Zhengzhou, Henan
450014, P.R. China.
(5)Department of Thoracic Surgery, The Affiliated Tumor Hospital of Zhengzhou
University (Henan Tumor Hospital), Zhengzhou, Henan 450008, P.R. China.
(6)Department of Urology, The Second Affiliated Hospital of Zhengzhou University,
Zhengzhou, Henan 450014, P.R. China.</i></span>
<span style="font-family: Arial, Helvetica, sans-serif;">
Berberine, an isoquinoline alkaloid extracted from the dry root of Coptidis Rhizoma, has been found to exhibit marked anticancer effects on a panel of established cancer cells. Among the human osteosarcoma lines treated, MG‑63 cells were found to be the most sensitive. The present study investigated the potential genotoxic effect of berberine on MG‑63 human osteosarcoma cells. The effect of berberine on cell viability was determined using a 3-(4,5-dimethylthiazol-2-yl)-2,5‑diphenyltetrazolium bromide assay and cell apoptosis was analyzed by flow cytometry and a DNA ladder assay. γH2AX focus formation was used to detect DNA damage in MG-63 cells. Berberine induced a significant increase in apoptosis in MG-63 cells in a concentration- and time-dependent manner, as determined by DNA fragmentation analysis and flow cytometry. Furthermore, berberine induced significant concentration- and time-dependent increases in DNA damage compared with that in the negative control. In conclusion, these observations indicated that berberine induced apoptosis and DNA damage in MG‑63 cells.</span>
<span style="font-family: Arial, Helvetica, sans-serif;">
</span>
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</pre>
Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com1tag:blogger.com,1999:blog-6407359362929739534.post-42977260136460858442014-11-17T13:01:00.003-08:002014-11-17T13:01:52.373-08:00Apigenin and Breast Cancer<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj07xYh6G9Hln5IZDRlxUh8XVW5Liw9WG9C0_z8LRncDAh8WXrtLhu7WXd4loV2HuBoQ53ZD5DY_14nh1mXZMWuEwre7A_dkMjq8wEWN5oAK38uuenjzbVMofoPhdn4oaiL5YONb_oSrCw/s1600/apigenin+and+breast+cancer+apoptosis.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj07xYh6G9Hln5IZDRlxUh8XVW5Liw9WG9C0_z8LRncDAh8WXrtLhu7WXd4loV2HuBoQ53ZD5DY_14nh1mXZMWuEwre7A_dkMjq8wEWN5oAK38uuenjzbVMofoPhdn4oaiL5YONb_oSrCw/s1600/apigenin+and+breast+cancer+apoptosis.jpg" height="153" width="200" /></a></div>
Several articles describing the apoptotic effects of apigenin in breast cancer cells.<br />
<br />
<h3>
1. Apigenin induced MCF-7 cell apoptosis-associated reactive oxygen species.</h3>
<br />
<a href="http://apigeninresearch.blogspot.com/">Apigenin</a> is a <a href="http://apigeninresearch.blogspot.com/2014/11/plant-flavonoids-kill-different-cancer-cells.html">flavonoid</a>, which has been proved to possess effective anti-cancer bioactivities against variety of cell lines. However, little is known about its effect on the cell-surface and the interaction between cell-surface and the reacting drug. In this study, human breast cancer line (MCF-7) was selected to be as a cell model to investigate the effects of apigenin on cell growth, proliferation, apoptosis, cellular morphology, etc. MTT assay showed that the growth inhibition induced by apigenin was in a dose-dependent manner when treated with different concentrations of apigenin while had little cytotoxic effects on human normal cells (MCF-10A). Fluorescence-based flow cytometry was used to detect cellular apoptosis and ROS production. The results showed that 80 µM apigenin could effectively induce apoptosis and overproduction of ROS in MCF-7 cells. Here, atomic force microscopy (AFM) was utilized to detect the shapes and membrane structures of MCF-7 cells at cellular or subcellular level. The results showed that the control MCF-7 cells presented typical elongated-spindle shapes with abundant pseudopodia, while after treated with apigenin, the cells shrunk and became round, the pseudopodia diminished. Moreover, the images of ultrastructure indicated that the cell membrane was composed of nanoparticles of 49?nm, but with the treated concentrations of apigenin increasing, the sizes of membrane particles significantly increased to 400?nm. These results can improve our understanding of apigenin, which can be potentially developed as a new agent for <a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">treatment of cancers</a>.<br />
<br />
<i>Bai H, Jin H, Yang F, Zhu H, Cai J. Apigenin induced MCF-7 cell apoptosis-associated reactive oxygen species. Scanning. 2014 Oct 18. doi: 10.1002/sca.21170. [Epub ahead of print] PubMed PMID: 25327419.</i><br />
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<br />
<h3>
2. Induction of caspase-dependent apoptosis by apigenin by inhibiting STAT3 signaling in HER2-overexpressing MDA-MB-453 breast cancer cells.</h3>
<br />
BACKGROUND: This study aimed to examine the effect of apigenin on proliferation and apoptosis in HER2-overexpressing MDA-MB-453 breast cancer cells.<br />
<br />
MATERIALS AND METHODS: The antiproliferative effects of apigenin were examined by proliferation and MTT assays. The effect of apigenin on apoptotic molecules was determined by western blotting. RT-PCR was performed to measure mRNA levels of HIF-1? and VEGF. ELISA assay was performed to measure intracellular VEGF levels. Immunocytochemistry was performed to evaluate nuclear STAT3 level.<br />
<br />
RESULTS: Apigenin inhibited the proliferation of MDA-MB-453 cells. Apigenin up-regulated the levels of cleaved caspase-8 and caspase-3, and induced the cleavage of PARP. Apigenin induced extrinsic apoptosis and blocked the activation (phosphorylation) of JAK2 and STAT3. Apigenin inhibited CoCl2-induced VEGF secretion and decreased the nuclear staining of STAT3.<br />
<br />
CONCLUSION: Apigenin exerts its antiproliferative activity by inhibiting STAT3 signaling. Apigenin could serve as a useful compound to prevent or treat HER2-overexpressing breast cancer.<br />
<br />
<i>Seo HS, Ku JM, Choi HS, Woo JK, Jang BH, Shin YC, Ko SG. Induction of caspase-dependent apoptosis by apigenin by inhibiting STAT3 signaling in HER2-overexpressing MDA-MB-453 breast cancer cells. Anticancer Res. 2014 Jun;34(6):2869-82. PubMed PMID: 24922650.</i><br />
<br />
<h3>
3. Effects of dietary apigenin on tumor latency, incidence and multiplicity in a medroxyprogesterone acetate-accelerated 7,12-dimethylbenz(a)anthracene-induced breast cancer model.</h3>
<br />
Medroxyprogesterone acetate (MPA) is a synthetic progestin commonly administered to postmenopausal women for hormone replacement therapy and has been associated with increased risk of breast cancer. MPA has been shown to accelerate the development of mammary tumors in a 7,12-dimethylbenz(a)anthracene (DMBA)-induced breast cancer animal model. Previously, we have shown that intraperitoneally administered apigenin effectively treated and prevented the progression of MPA-accelerated breast cancer in DMBA-induced and xenograft mammary cancer models. Here we used the DMBA model to examine the chemopreventive effect of dietary apigenin against MPA-accelerated tumors with 3 different levels of apigenin (0.02%, 0.1%, and 0.5% w/w) incorporated into a phytoestrogen-free diet. Results showed that 0.1% dietary apigenin reduced MPA-dependent tumor incidence; however, the same dietary level increased tumor multiplicity in animals that developed tumors. Neither 0.02% nor 0.5% dietary apigenin reduced MPA-dependent tumor incidence or latency, and tumor multiplicity increased significantly in response to 0.5% apigenin. These results contrast with previous chemopreventive effects observed when apigenin was administered intraperitoneally, suggesting that route of administration may influence its action. Consequently, until further research clarifies the effect of dietary apigenin on progestin-accelerated mammary tumors, caution should be exercised when considering the flavonoid as a dietary supplement for preventing hormone-dependent breast cancer.<br />
<br />
<i>Mafuvadze B, Cook M, Xu Z, Besch-Williford CL, Hyder SM. Effects of dietary apigenin on tumor latency, incidence and multiplicity in a medroxyprogesterone acetate-accelerated 7,12-dimethylbenz(a)anthracene-induced breast cancer model. Nutr Cancer. 2013;65(8):1184-91. doi: 10.1080/01635581.2013.833637. Epub 2013 Oct 15. PubMed PMID: 24127693.</i><br />
<br />
<h3>
4. Autophagy inhibition enhances apigenin-induced apoptosis in human breast cancer cells.</h3>
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Apigenin (4',5,7-trihydroxyflavone) is a member of the flavone subclass of flavonoids present in fruits and vegetables. The involvement of autophagy in the apigenin-induced apoptotic death of human breast cancer cells was investigated. Cell proliferation and viability were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and clonogenic assays. Flow cytometry, fluorescent staining and Western blot analysis were employed to detect apoptosis and autophagy, and the role of autophagy was assessed using autophagy inhibitors. Apigenin dose- and time-dependently repressed the proliferation and clonogenic survival of the human breast cancer T47D and MDA-MB-231 cell lines. The death of T47D and MDA-MB-231 cells was due to apoptosis associated with increased levels of Caspase3, PARP cleavage and Bax/Bcl-2 ratios. The results from flow cytometry and fluorescent staining also verified the occurrence of apoptosis. In addition, the apigenin-treated cells exhibited autophagy, as characterized by the appearance of autophagosomes under fluorescence microscopy and the accumulation of acidic vesicular organelles (AVOs) by flow cytometry. Furthermore, the results of the Western blot analysis revealed that the level of LC3-II, the processed form of LC3-I, was increased. Treatment with the autophagy inhibitor, 3-methyladenine (3-MA), significantly enhanced the apoptosis induced by apigenin, which was accompanied by an increase in the level of PARP cleavage. Similar results were also confirmed by flow cytometry and fluorescence microscopy. These results indicate that apigenin has apoptosis- and autophagy-inducing effects in breast cancer cells. Autophagy plays a cyto-protective role in apigenin-induced apoptosis, and the combination of apigenin and an autophagy inhibitor may be a promising strategy for breast cancer control.<br />
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<i>Cao X, Liu B, Cao W, Zhang W, Zhang F, Zhao H, Meng R, Zhang L, Niu R, Hao X, Zhang B. Autophagy inhibition enhances apigenin-induced apoptosis in human breast cancer cells. Chin J Cancer Res. 2013 Apr;25(2):212-22. doi:10.3978/j.issn.1000-9604.2013.04.01. PubMed PMID: 23592903; PubMed </i><br />
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5. Apigenin induces apoptosis and blocks growth of medroxyprogesterone acetate-dependent BT-474 xenograft tumors.</h3>
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Recent clinical and epidemiological evidence shows that hormone replacement therapy (HRT) containing both estrogen and progestin increases the risk of primary and metastatic breast cancer in post-menopausal women while HRT containing only estrogen does not. We and others previously showed that progestins promote the growth of human breast cancer cells in vitro and in vivo. In this study, we sought to determine whether apigenin, a low molecular weight anti-carcinogenic flavonoid, inhibits the growth of aggressive Her2/neu-positive BT-474 xenograft tumors in nude mice exposed to medroxyprogesterone acetate (MPA), the most commonly used progestin in the USA. Our data clearly show that apigenin (50 mg/kg) inhibits progression and development of these xenograft tumors by inducing apoptosis, inhibiting cell proliferation, and reducing expression of Her2/neu. Moreover, apigenin reduced levels of vascular endothelial growth factor (VEGF) without altering blood vessel density, indicating that continued expression of VEGF may be required to promote tumor cell survival and maintain blood flow. While previous studies showed that MPA induces receptor activator of nuclear factor kappa-B ligand (RANKL) expression in rodent mammary gland, MPA reduced levels of RANKL in human tumor xenografts. RANKL levels remained suppressed in the presence of apigenin. Exposure of BT-474 cells to MPA in vitro also resulted in lower levels of RANKL; an effect that was independent of progesterone receptors since it occurred both in the presence and absence of the antiprogestin RU-486. In contrast to our in vivo observations, apigenin protected against MPA-dependent RANKL loss in vitro, suggesting that MPA and apigenin modulate RANKL levels differently in breast cancer cells in vivo and in vitro. These preclinical findings suggest that apigenin has potential as an agent for the treatment of progestin-dependent breast disease.<br />
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<i>Mafuvadze B, Liang Y, Besch-Williford C, Zhang X, Hyder SM. Apigenin induces apoptosis and blocks growth of medroxyprogesterone acetate-dependent BT-474 xenograft tumors. Horm Cancer. 2012 Aug;3(4):160-71. doi: 10.1007/s12672-012-0114-x. Epub 2012 May 9. PubMed PMID: 22569706.</i><br />
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6. Apigenin induces apoptosis via extrinsic pathway, inducing p53 and inhibiting STAT3 and NF?B signaling in HER2-overexpressing breast cancer cells.</h3>
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Phytoestrogens are known to prevent tumor induction. But their molecular mechanisms of action are still unknown. This study aimed to examine the effect of apigenin on proliferation and apoptosis in HER2-expressing breast cancer cells. In our experiments, apigenin inhibited the proliferation of MCF-7 vec and MCF-7 HER2 cells. This growth inhibition was accompanied with an increase of sub G(0)/G(1) apoptotic fractions. Overexpression of HER2 did not confer resistance to apigenin in MCF-7 cells. Apigenin-induced extrinsic apoptosis pathway up-regulating the levels of cleaved caspase-8, and inducing the cleavage of poly (ADP-ribose) polymerase, whereas apigenin did not induce apoptosis via intrinsic mitochondrial apoptosis pathway since this compound did not decrease mitochondrial membrane potential maintaining red fluorescence and did not affect the levels of B-cell lymphoma 2 (BCL2) and Bcl-2-associated X protein. Moreover, apigenin reduced the tyrosine phosphorylation of HER2 (phospho-HER2 level) in MCF-7 HER2 cells, and up-regulated the levels of p53, phospho-p53 and p21 in MCF-7 vec and MCF-7 HER2 cells. This suggests that apigenin induces apoptosis through p53-dependent pathway. Apigenin also reduced the expression of phospho-JAK1 and phospho-STAT3 and decreased STAT3-dependent luciferase reporter gene activity in MCF-7 vec and MCF-7 HER2 cells. Apigenin decreased the phosphorylation level of I?B? in the cytosol, and abrogated the nuclear translocation of p65 within the nucleus suggesting that it blocks the activation of NF?B signaling pathway in MCF-7 vec and MCF-7 HER2 cells. Our study indicates that apigenin could be a potential useful compound to prevent or treat HER2-overexpressing breast cancer.<br />
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<i>Seo HS, Choi HS, Kim SR, Choi YK, Woo SM, Shin I, Woo JK, Park SY, Shin YC, Ko SG. Apigenin induces apoptosis via extrinsic pathway, inducing p53 and inhibiting STAT3 and NF?B signaling in HER2-overexpressing breast cancer cells. Mol Cell Biochem. 2012 Jul;366(1-2):319-34. doi: 10.1007/s11010-012-1310-2.</i><br />
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<b>7. Apigenin prevents development of medroxyprogesterone acetate-accelerated 7,12-dimethylbenz(a)anthracene-induced mammary tumors in Sprague-Dawley rats.</b><br />
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The use of progestins as a component of hormone replacement therapy has been linked to an increase in breast cancer risk in postmenopausal women. We have previously shown that medroxyprogesterone acetate (MPA), a commonly administered synthetic progestin, increases production of the potent angiogenic factor vascular endothelial growth factor (VEGF) by tumor cells, leading to the development of new blood vessels and tumor growth. We sought to identify nontoxic chemicals that would inhibit progestin-induced tumorigenesis. We used a recently developed progestin-dependent mammary cancer model in which tumors are induced in Sprague-Dawley rats by 7,12-dimethylbenz(a)anthracene (DMBA) treatment. The flavonoid apigenin, which we previously found to inhibit progestin-dependent VEGF synthesis in human breast cancer cells in vitro, significantly delayed the development of, and decreased the incidence and multiplicity of, MPA-accelerated DMBA-induced mammary tumors in this animal model. Whereas apigenin decreased the occurrence of such tumors, it did not block MPA-induced intraductal and lobular epithelial cell hyperplasia in the mammary tissue. Apigenin blocked MPA-dependent increases in VEGF, and suppressed VEGF receptor-2 (VEGFR-2) but not VEGFR-1 in regions of hyperplasia. No differences were observed in estrogen or progesterone receptor (ER/PR) levels, or the number of estrogen receptor-positive cells, within the mammary gland of MPA-treated animals administered apigenin, MPA-treated animals, and placebo treated animals. However, the number of progesterone receptor-positive cells was reduced in animals treated with MPA or MPA and apigenin compared with those treated with placebo. These findings suggest that apigenin has important chemopreventive properties for those breast cancers that develop in response to progestins.<br />
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<i>Mafuvadze B, Benakanakere I, López Pérez FR, Besch-Williford C, Ellersieck MR, Hyder SM. Apigenin prevents development of medroxyprogesterone acetate-accelerated 7,12-dimethylbenz(a)anthracene-induced mammary tumors in Sprague-Dawley rats. Cancer Prev Res (Phila). 2011 Aug;4(8):1316-24. doi: 10.1158/1940-6207.CAPR-10-0382. </i><br />
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8. The dietary flavonoid apigenin blocks phorbol 12-myristate 13-acetate-induced COX-2 transcriptional activity in breast cell lines.</h3>
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<a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">Cyclooxygenase (COX)-2</a> is the inducible isozyme catalyzing the conversion of arachidonic acid to prostanoids. Its expression has been linked to the process of carcinogenesis, including tumorigenesis of the breast. Apigenin (APG) is a flavone commonly found in fruit and vegetables, and is shown to be a potential modulator in inflammatory diseases. This study examined the potential suppressive effect of the flavone on phorbol ester-induced COX-2 expression in the breast cell lines MCF-10A and MCF-7. Real-time PCR and/or Western blotting indicated that APG in micromolar range significantly inhibited phorbol 12-myristate 13-acetate (PMA)-induced COX-2 expression in these breast cells. APG treatment reduced the amount of phospho-mitogen-activated protein kinase (MAPK) ERK-1/2, but it did not alter the activity of PKC. Activated ERKs might trigger the transactivation of AP-1 or CRE, which can be located at COX-2 promoter region (-72/-53). Reporter gene assay as well as electrophoretic mobility shift assays (EMSA) illustrated that APG inhibited transcription factor binding at this region in a dose-dependent manner. This study showed that APG down-regulated PMA-induced COX-2 expression in breast cells without affecting PKC activity. These findings could provide a scientific basis for developing APG nutraceutical against breast carcinogenesis.<br />
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<i>Yi Lau GT, Leung LK. The dietary flavonoid apigenin blocks phorbol 12-myristate 13-acetate-induced COX-2 transcriptional activity in breast cell lines. Food Chem Toxicol. 2010 Oct;48(10):3022-7. doi: 10.1016/j.fct.2010.07.046. Epub 2010 Aug 4. PubMed PMID: 20691240.</i><br />
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Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-75145516028130957892014-11-14T13:16:00.000-08:002014-11-14T13:20:13.522-08:00Apigenin and Prostate Cancer - recently published 6 articles <div class="separator" style="clear: both; text-align: center;">
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Selected apigenin papers devoted to investigate its antiproliferative effect in cancer cells including prostate cancer and to analyze molecular response of the cells, published in 2014.<br />
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1. Regulation of GLUT transporters by flavonoids in androgen-sensitive and-insensitive prostate cancer cells.</h4>
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Cancer cells show different metabolic requirements from normal cells. In prostate cancer, particularly, glycolytic metabolism differs in androgen-responsive and nonresponsive cells. In addition, some natural compounds with antiproliferative activities are able to modify glucose entry into cells by either modulating glucose transporter (GLUT) expression or by altering glucose binding.<br />
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The aim of this work was to study the regulation of some GLUTs (GLUT1 and GLUT4) in both androgen-sensitive (LNCaP) and -insensitive (PC-3) prostate cancer cells by 4 structurally different flavonoids (ie, genistein, phloretin, apigenin, and daidzein).<br />
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Glucose uptake was measured using nonradiolabeled 2-deoxyglucose. The evaluation of protein levels as well as subcellular distribution of GLUT1/4 were analyzed by Western blot and immunocytochemistry, respectively. Androgen-insensitive LNCaP-R and androgen-sensitive PC-3-AR cells were used to study the effect of androgen signaling. Additionally, a docking simulation was employed to compare interactions between flavonoids and XylE, a bacterial homolog of GLUT1 to -4.<br />
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<b>Results show for the first time the presence of functionally relevant GLUT4 in prostate cancer cells. </b>Furthermore, differences in GLUT1 and GLUT4 levels and glucose uptake were found, without differences on subcellular distribution, after incubation with flavonoids. Docking simulation showed that all compounds interact with the same location of transporters. More importantly, differences between androgen-sensitive and -insensitive prostate cancer cells were found in both GLUT protein levels and glucose uptake.<br />
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<b>Thus, phenotypic characteristics of prostate cancer cells are responsible for the different effects of these flavonoids in glucose uptake and in GLUT expression rather than their structural differences, with the most effective in reducing cell growth being the highest in modifying glucose uptake and GLUT levels.</b><br />
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<i>Gonzalez-Menendez P, Hevia D, Rodriguez-Garcia A, Mayo JC, Sainz RM. Regulation of GLUT transporters by flavonoids in androgen-sensitive and -insensitive prostate cancer cells. Endocrinology. 2014 Sep;155(9):3238-50. doi: 10.1210/en.2014-1260. </i><br />
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2. Plant flavone apigenin binds to nucleic acid bases and reduces oxidative DNA damage in prostate epithelial cells.</h4>
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Oxidative stress has been linked to prostate carcinogenesis as human prostate tissue is vulnerable to oxidative DNA damage. Apigenin, a dietary plant flavone, possesses anti-proliferative and anticancer effects; however, its antioxidant properties have not been fully elucidated.<br />
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We investigated sub-cellular distribution of apigenin, it's binding to DNA and protective effects against H2O2-induced DNA damage using transformed human prostate epithelial RWPE-1 cells and prostate cancer LNCaP, PC-3 and DU145 cells. Exposure of cells to apigenin exhibited higher accumulation in RWPE-1 and LNCaP cells, compared to PC-3 and DU145 cells.<br />
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The kinetics of apigenin uptake in LNCaP cells was estimated with a Km value of 5 µmole/L and Vmax of 190 pmoles/million cells/h. Sub-cellular fractionation demonstrated that nuclear matrix retains the highest concentration of apigenin (45.3%), followed by cytosol (23.9%), nuclear membranes (17.9%) and microsomes (12.9%), respectively.<br />
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Spectroscopic analysis of apigenin with calf-thymus DNA exhibited intercalation as the dominant binding mode to DNA duplex. Apigenin exposure resulted in significant genoprotective effects in H2O2-stressed RWPE-1 cells by reduction in reactive oxygen species levels.<br />
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In addition, apigenin exposure suppressed the formation of 8-hydroxy-2' deoxyguanosine and protected exposed cells from apoptosis.<br />
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Our studies demonstrate that<b> apigenin is readily taken up by normal prostatic epithelial cells and prostate cancer cells, and is incorporated into their nuclei</b>, where its intercalation with nucleic acid bases may account for its <a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">antioxidant and chemopreventive</a> activities.<br />
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<i>Sharma H, Kanwal R, Bhaskaran N, Gupta S. Plant flavone apigenin binds to nucleic acid bases and reduces oxidative DNA damage in prostate epithelial cells. PLoS One. 2014 Mar 10;9(3):e91588. doi: 10.1371/journal.pone.0091588. eCollection 2014. </i><br />
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3. Apigenin induces apoptosis by targeting inhibitor of apoptosis proteins and Ku70-Bax interaction in prostate cancer.</h4>
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Dysfunction of the apoptotic pathway in prostate cancer cells confers apoptosis resistance towards various therapies. A novel strategy to overcome resistance is to directly target the apoptotic pathway in cancer cells. Apigenin, an anticancer agent, selectively toxic to cancer cells induces cell cycle arrest and apoptosis through mechanisms which are not fully explored.<br />
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In the present study we provide novel insight into the mechanisms of apoptosis induction by apigenin.<br />
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Treatment of androgen-refractory human prostate cancer PC-3 and DU145 cells with apigenin resulted in dose-dependent suppression of XIAP, c-IAP1, c-IAP2 and survivin protein levels. Apigenin treatment resulted in significant decrease in cell viability and apoptosis induction with the increase of cytochrome C in time-dependent manner.<br />
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These effects of apigenin were accompanied by decrease in Bcl-xL and Bcl-2 and increase in the active form of Bax protein. The apigenin-mediated increase in Bax was due to dissociation of Bax from Ku70 which is essential for apoptotic activity of Bax.<br />
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Apigenin treatment resulted in the inhibition of class I histone deacetylases and HDAC1 protein expression, thereby increasing the acetylation of Ku70 and the dissociation of Bax resulting in apoptosis of cancer cells.<br />
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Furthermore, apigenin significantly reduced HDAC1 occupancy at the XIAP promoter, suggesting that histone deacetylation might be critical for XIAP downregulation.<br />
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These results suggest that <b>apigenin targets inhibitor of apoptosis proteins and Ku70-Bax interaction in the induction of apoptosis in prostate cancer cells</b> and in athymic nude mouse xenograft model endorsing its in vivo efficacy.<br />
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<i>Shukla S, Fu P, Gupta S. Apigenin induces apoptosis by targeting inhibitor of apoptosis proteins and Ku70-Bax interaction in prostate cancer. Apoptosis. 2014 May;19(5):883-94. doi: 10.1007/s10495-014-0971-6.</i><br />
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5. Apigenin inhibits prostate cancer progression in TRAMP mice via targeting PI3K/Akt/FoxO pathway.</h4>
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Forkhead box O (FoxO) transcription factors play an important role as tumor suppressor in several human malignancies. Disruption of FoxO activity due to loss of phosphatase and tensin homolog and activation of phosphatidylinositol-3 kinase (PI3K)/Akt are frequently observed in prostate cancer. Apigenin, a naturally occurring plant flavone, exhibits antiproliferative and anticarcinogenic activities through mechanisms, which are not fully defined.<br />
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In the present study, we show that apigenin suppressed prostate tumorigenesis in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice through the PI3K/Akt/FoxO-signaling pathway.<br />
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Apigenin-treated TRAMP mice (20 and 50 µg/mouse/day, 6 days/week for 20 weeks) exhibited significant decrease in tumor volumes of the prostate as well as completely abolished distant organ metastasis. Apigenin treatment resulted in significant decrease in the weight of genitourinary apparatus (P < 0.0001), dorsolateral (P < 0.0001) and ventral prostate (P < 0.028), compared with the control group.<br />
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Apigenin-treated mice showed reduced phosphorylation of Akt (Ser473) and FoxO3a (Ser253), which correlated with its increased nuclear retention and decreased binding of FoxO3a with 14-3-3. These events lead to reduced proliferation as assessed by Ki-67 and cyclin D1, along with upregulation of FoxO-responsive proteins BIM and p27/Kip1. <br />
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Complementing in vivo results, similar observations were noted in human prostate cancer LNCaP and PC-3 cells after apigenin treatment. Furthermore, binding of FoxO3a with p27/Kip1 was markedly increased after 10 and 20 µM apigenin treatment resulting in G0/G1-phase cell cycle arrest, which was consistent with the effects elicited by PI3K/Akt inhibitor, LY294002.<br />
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<b>These results provide convincing evidence that apigenin effectively suppressed prostate cancer progression, at least in part, by targeting the PI3K/Akt/FoxO-signaling pathway.</b><br />
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<i>Shukla S, Bhaskaran N, Babcook MA, Fu P, Maclennan GT, Gupta S. Apigenin inhibits prostate cancer progression in TRAMP mice via targeting PI3K/Akt/FoxO pathway. Carcinogenesis. 2014 Feb;35(2):452-60. doi: 10.1093/carcin/bgt316.</i><br />
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6. Axl receptor tyrosine kinase is a novel target of apigenin for the inhibition of cell proliferation.</h4>
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The Axl receptor tyrosine kinase (RTK), along with Tyro 3 and Mer, belongs to the TAM subfamily that promotes survival, stimulates proliferation and/or inhibits apoptosis. In various types of human cancer, including breast, lung and prostate cancer, Axl expression is increased and correlates with an advanced clinical stage.<br />
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In this study, we examined whether apigenin has an effect on Axl expression, which in turn can affect cell proliferation. The treatment of the non-small cell lung cancer (NSCLC) cells, A549 and H460, with apigenin decreased Axl mRNA and protein expression in a dose-dependent manner. Axl promoter activity was also inhibited by apigenin, indicating that apigenin suppressed Axl expression at the transcriptional level.<br />
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Upon treatment with apigenin, the viability of both the A549 and H460 cells was gradually decreased and the anti-proliferative effects were further confirmed by the dose-dependent decrease in the clonogenic ability of the apigenin-treated cells.<br />
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Subsequently, we found that the viability and clonogenic ability of the cells treated with apigenin was less or more affected by transfection of the cells with a Axl-expressing plasmid or Axl targeting siRNA, compared to transfection with the empty vector or control siRNA, respectively. In addition, apigenin increased the expression of p21, a cyclin-dependent kinase inhibitor, but reduced the expression of X-linked inhibitor of apoptosis protein (XIAP).<br />
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These cell cycle arrest and pro-apoptotic effects of apigenin were also attenuated or augmented by the up- or downregulation of Axl expression, respectively, which suggests that Axl is a novel target of apigenin through which it exerts its inhibitory effects on cell proliferation.<br />
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Taken together, our data indicate that <b>apigenin downregulates Axl expression, which subsequently results in the inhibition of NSCLC cell proliferation through the increase and decrease of p21 and XIAP expression</b>, respectively.<br />
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<i>Kim KC, Choi EH, Lee C. Axl receptor tyrosine kinase is a novel target of apigenin for the inhibition of cell proliferation. Int J Mol Med. 2014 Aug;34(2):592-8. doi: 10.3892/ijmm.2014.1804. </i><br />
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<br />Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-80734220906078512014-11-09T15:30:00.000-08:002014-11-12T10:49:57.379-08:00Apigenin induced ATF3 to decrease ER stress-induced chemokine expression by epigenetically supression of EGR1 expression<div class="separator" style="clear: both; text-align: center;">
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New research published in the “Journal of Biological Chemistry”, showed in <a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">intestinal cancer cells, apigenin</a> induced ATF3 upregulation and this effect diminished <b>endoplasmic reticulum (ER) stress</b> response via <b>epigenetically supression of EGR1 expression</b>.<br />
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The abstract of the recent research paper dedicated to investigate the relationship between <i>apigenin and ER stress induced cancer chemokine expression</i> was given below. You can check the article, written by Dr. Park and colleagues, using the link provided below of this post.<br />
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<h3>
Activating Transcription Factor 3-mediated Chemo-intervention with Cancer Chemokines in a Noncanonical Pathway under Endoplasmic Reticulum Stress</h3>
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The cell-protective features of the endoplasmic reticulum (ER) stress response are chronically activated in vigorously <b>growing malignant tumor cells</b>, which provide cellular growth advantages over the adverse microenvironment including chemotherapy. As an intervention with ER stress responses in the intestinal cancer cells, preventive exposure to <b>flavone apigenin</b> potentiated superinduction of a regulatory transcription factor, activating transcription factor 3 (ATF3), which is also known to be an integral player coordinating ER stress response-related gene expression.<br />
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<b>Results</b><br />
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ATF3 superinduction was due to increased turnover of ATF3 transcript via stabilization with HuR protein in the <b>cancer cells under ER stress</b>. Moreover, enhanced ATF3 caused inhibitory action against ER stress-induced cancer chemokines that are potent mediators determining the survival and metastatic potential of epithelial cancer cells. Although enhanced ATF3 was a negative regulator of the well known proinflammatory transcription factor NF-kB, blocking of NF-?B signaling did not affect ER stress-induced chemokine expression. Instead, immediately expressed transcription factor early growth response protein 1 (EGR-1) was positively involved in cancer chemokine induction by ER stressors. ER stress-induced EGR-1 and subsequent chemokine production were repressed by ATF3. Mechanistically, ATF3 directly interacted with and recruited HDAC1 protein, which led to epigenetic suppression of EGR-1 expression and subsequent chemokine production.<br />
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<b>Conclusion</b><br />
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Conclusively, superinduced ATF3 attenuated ER stress-induced cancer chemokine expression by epigenetically interfering with induction of EGR-1, a transcriptional modulator crucial to cancer chemokine production. <b>Thus, these results suggest a potent therapeutic intervention of ER stress response-related cancer-favoring events by ATF3.</b><br />
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<b>Reference</b><br />
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Park SH, Kim J, Do KH, Park J, Oh CG, Choi HJ, Song BG, Lee SJ, Kim YS, Moon Y. Activating Transcription Factor 3-mediated Chemo-intervention with Cancer Chemokines in a Noncanonical Pathway under Endoplasmic Reticulum Stress. <a href="http://www.ncbi.nlm.nih.gov/pubmed/25122760">J Biol Chem. 2014 Sep 26;289(39):27118-33</a>. doi: 10.1074/jbc.M114.568717.<br />
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Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-43622554161752456672014-11-09T12:00:00.000-08:002014-11-12T10:50:27.363-08:00Plant flavonoids kill different cancer types<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhowndEEvxWpD3SELBahof5yOah6uYW46BpJUrX2zsyOy5CJ9WSwam0SCK7j0K1vFzsPXeMLnRzsjNw16SFSUJy-RSITSh0x7sQHBq2CJ9WqXQrka6VkiMP2VkoSYTOBxWAO_cVXTgaWlA/s1600/adult-84478__180.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="herbs with apigenin kills cancer cells" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhowndEEvxWpD3SELBahof5yOah6uYW46BpJUrX2zsyOy5CJ9WSwam0SCK7j0K1vFzsPXeMLnRzsjNw16SFSUJy-RSITSh0x7sQHBq2CJ9WqXQrka6VkiMP2VkoSYTOBxWAO_cVXTgaWlA/s1600/adult-84478__180.jpg" height="159" title="flavonoids fight cancer" width="200" /></a></div>
A recent review published in the Pharmacognosy Reviews journal summarize the<b> cancer killing effects</b> of several <a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">flavonoids, including apigenin, chrysin, luteolin</a> and many others. Here is the abstract of the article published, you can check this by clicking the link below. <br />
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Dr. Katrin Sak, recently reviewed <b>cytotoxic effects of several plant flavonoids, including apigenin, chrysin, luteolin and many others</b>.<br />
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<h3>
Cytotoxicity of dietary flavonoids on different human cancer types</h3>
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<b>Flavonoids</b> are ubiquitous in nature. They are also in food, providing an essential link between diet and prevention of chronic diseases including cancer. Anticancer effects of these polyphenols depend on several factors: <b>Their chemical structure and concentration, and also on the type of cancer.</b><br />
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<b>Malignant cells from different tissues</b> reveal somewhat different sensitivity toward flavonoids and, therefore, the preferences of the <b>most common dietary flavonoids</b> to various human cancer types are analyzed in this review. While luteolin and kaempferol can be considered as promising candidate agents for treatment of gastric and ovarian cancers, respectively, <b>apigenin, chrysin, and luteolin</b> have good perspectives as potent <b><a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">antitumor agents for cervical cancer</a></b>; cells from main sites of <b>flavonoid metabolism </b>(colon and liver) reveal rather large fluctuations in anticancer activity probably due to exposure to various metabolites with different activities.<br />
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<b>Anticancer effect of flavonoids toward blood cancer cells depend on their myeloid, lymphoid, or erythroid origin;</b> <i>cytotoxic effects of flavonoids on breast and prostate cancer cells are highly related to the expression of hormone receptors.</i> Different flavonoids are often preferentially present in certain food items, and knowledge about the malignant tissue-specific anticancer effects of flavonoids could be purposely applied both in <a href="http://apigeninresearch.blogspot.com/">chemoprevention</a> as well as in cancer treatment.<br />
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<b>Reference</b><br />
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Sak K. Cytotoxicity of dietary flavonoids on different human cancer types.<br />
Pharmacogn Rev. 2014 Jul;8(16):122-46. doi: <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4127821/">10.4103/0973-7847.134247</a>.<br />
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<a href="http://apigeninresearch.blogspot.com/2014/11/apigenin-affects-human-prostate-cancer.html">Apigenin and prostate cancer treatment</a><br />
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<a href="http://apigeninresearch.blogspot.com/2014/11/apigenin-triggers-breast-cancer-death.html">Apigenin causes apoptotic death of breast cancer cell</a>Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-66144468408323579512014-11-02T10:30:00.000-08:002014-11-12T10:54:40.177-08:00Apigenin affects human prostate cancer cells<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh7CL23ZxK0MBW7I-bmqV0hryf2cVsVGFYw2uSfelhCyyOyK7Ik0-YN_Eey4P-ujV2QlBwvK0igFoaHckI6Yt9uMjSuloG6jrkAzgM9UwC8HvBz9TB5qIHKQ2G1j2QOmg2PMG2OctTFYl8/s1600/prostate-cancer-cells.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh7CL23ZxK0MBW7I-bmqV0hryf2cVsVGFYw2uSfelhCyyOyK7Ik0-YN_Eey4P-ujV2QlBwvK0igFoaHckI6Yt9uMjSuloG6jrkAzgM9UwC8HvBz9TB5qIHKQ2G1j2QOmg2PMG2OctTFYl8/s1600/prostate-cancer-cells.jpg" height="177" width="320" /></a></div>
<b>Apigenin modulates EMT in prostate cancer cells (DU145)</b> <b>and this</b> <b>results in suppression of cell proliferation and inhibition of cell migration and invasive potential, </b>a new study showed published Molecular Medicine Reports.<br />
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Apigenin inhibits migration and invasion via modulation of epithelial mesenchymal transition in prostate cancer</h4>
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<b>Abstract of the Article </b><br />
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The mortality rate associated with <b>prostate cancer</b> is mainly due to <b>metastases</b> rather than primary organ confined disease. Decreasing the incidence of metastasis is important in treating prostate cancer. <b>4',5,7 trihydroxyflavone (apigenin)</b> has been demonstrated to be effective in inhibiting several types of cancer.<br />
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The aim of this study was to investigate the effect and mechanism of apigenin on the <b>movement of prostate cancer cells</b>. In the present study, DU145 cells were treated with varying concentrations of apigenin for different time periods.<br />
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<b>Cell viability</b> was evaluated using an MTT assay. <i>Cell motility and invasiveness were assayed using wound healing assays and a Matrigel migration and invasion assay.</i> <b>Flow cytometric and western blot analyses</b> were performed to examine the cell cycle and signaling pathways.<br />
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The results demonstrated that apigenin suppressed the proliferation and inhibited the migration and invasive potential of the DU145 prostate cancer cells in a dose and time dependent manner, which was associated with epithelial mesenchymal transition.<br />
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<b><i>These findings suggested that apigenin may be effective in treating human prostate cancer.</i></b><br />
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Original Article<br />
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Zhu Y, Wu J, Li S, Wang X, Liang Z, Xu X, Xu X, Hu Z, Lin Y, Chen H, Qin J, Mao Q, Xie L. Apigenin inhibits migration and invasion via modulation of epithelial mesenchymal transition in prostate cancer. <a href="http://www.spandidos-publications.com/10.3892/mmr.2014.2801" rel="nofollow" target="_blank">Mol Med Rep. 2014 Oct 29</a>. doi: 10.3892/mmr.2014.2801. [Epub ahead of print] PubMed PMID: 25351792.<br />
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<a href="http://apigeninresearch.blogspot.com/2014/11/apigenin-triggers-breast-cancer-death.html">Apigenin: Breast cancer cell apoptosis and ROS production</a><br />
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<a href="http://apigeninresearch.blogspot.com/2014/10/apigenin-in-damiana-kills-breast-cancer-cells.html">Apigenin in Damiana Fights Breast Cancer Cells</a><br />
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<a href="http://apigeninresearch.blogspot.com/2014/10/products-of-indonesian-stingless-bee.html">Propolis of Indonesian stingless bee kill human cancer cells</a></div>
Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-74541672841796537492014-11-01T13:45:00.000-07:002014-11-12T10:55:11.123-08:00Apigenin triggers breast cancer cell apoptosis and ROS production<div class="MsoNormal">
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi-u1zPhgsN6xT-EOnp8U7wbXNk6tRVhPSa5zZARwSSRn8ITITPIP0Ip6Pp1nhIpfzGj7KNGtP71Glh4yVihxIxmgI9ISBFt-hBz1bw7ZbAGQEGOtci5okML7YT-jDCDpdy-Dn-t6IW2Go/s1600/cancer+cell-apigenin.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="apigenin role in breast cancers" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi-u1zPhgsN6xT-EOnp8U7wbXNk6tRVhPSa5zZARwSSRn8ITITPIP0Ip6Pp1nhIpfzGj7KNGtP71Glh4yVihxIxmgI9ISBFt-hBz1bw7ZbAGQEGOtci5okML7YT-jDCDpdy-Dn-t6IW2Go/s1600/cancer+cell-apigenin.jpg" height="200" title="apigenin and MCF7 cells" width="200" /></a></div>
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Another <a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">anti-cancer activity of apigenin</a> has been was shown in breast cancer cells. <a href="http://apigeninresearch.blogspot.com/">Apigenin</a> was found to effectively induce
apoptotic cell death and overproduction of reactive oxygen species in breast
cancer cells, MCF-7 cells, in the article recently published in Scanning
journal.</div>
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<h4>
Apigenin induced MCF-7 cell apoptosis-associated reactive oxygen species.</h4>
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<i>Abstract of the article</i><o:p></o:p></div>
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<b>Apigenin is a flavonoid,</b> which has been proved to possess
effective anti-cancer bioactivities against variety of cell lines. However,
little is known about its effect on the cell-surface and the interaction
between cell-surface and the reacting drug. </div>
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In this study, <b>human breast cancer
line (MCF-7)</b> was selected to be as a cell model to investigate the effects of
apigenin on <b>cell growth, proliferation, apoptosis, cellular morphology</b>, etc.
MTT assay showed that the growth inhibition induced by apigenin was in a
dose-dependent manner when treated with different concentrations of apigenin
<b>while had little cytotoxic effects on human normal cells (MCF-10A)</b>.
Fluorescence-based flow cytometry was used to detect cellular apoptosis and ROS
production. </div>
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The results showed that <b>80 µM apigenin</b> could effectively
induce apoptosis and overproduction of ROS in <b>MCF-7 cells</b>. Here, <b>atomic force
microscopy</b> (AFM) was utilized to detect the shapes and membrane structures of
<b>MCF-7 cells</b> at cellular or subcellular level. </div>
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The results showed that the control <b>MCF-7 cells</b> presented
typical elongated-spindle shapes with abundant pseudopodia, while after treated
with apigenin, the cells shrunk and became round, the pseudopodia diminished.
Moreover, the images of ultrastructure indicated that the cell membrane was
composed of nanoparticles of 49 nm, but with the treated concentrations of
apigenin increasing, the sizes of membrane particles significantly increased to
400 nm. </div>
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<b>These results can improve our understanding of apigenin,
which can be potentially developed as a new agent for treatment of cancers.</b></div>
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Please share this article using below links.</div>
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Original Article:</div>
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Bai H, Jin H, Yang F, Zhu H, Cai J. Apigenin induced MCF-7 cell apoptosis-associated reactive oxygen species. <a href="http://dx.doi.org/10.1002/sca.21170">Scanning</a>. 2014 Oct 18. doi:10.1002/sca.21170. [Epub ahead of print] PubMed PMID: 25327419.</div>
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<a href="http://apigeninresearch.blogspot.com/2014/10/apigenin-in-damiana-kills-breast-cancer-cells.html">Damiana Kills Breast Cancer Cells</a><br />
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<a href="http://apigeninresearch.blogspot.com/2014/10/products-of-indonesian-stingless-bee.html">Indonesian stingless bee vs human cancer cells</a><br />
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<a href="http://apigeninresearch.blogspot.com/2014/10/combined-apigenin-and-barasertib.html">Apigenin plus barasertib treatment can overcome cetuximab resistance</a><br />
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Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-3411002199766375322014-10-17T14:10:00.000-07:002014-11-12T10:52:56.816-08:00Apigenin in Damiana Kills Breast Cancer Cells<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjpNXzX3Tt5dFidi_siquuJRf0gNGKNcqp28vVNuRSWZZtU-gayBOcjCsfSdCLwVlVYkNzCca6OOdm_89lwcycjMzDub1FSIy2yeujY14cZuJkgOjP867BWGpzym0UFo1m7eG-Mv53-JTM/s1600/damiana-apigenin.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjpNXzX3Tt5dFidi_siquuJRf0gNGKNcqp28vVNuRSWZZtU-gayBOcjCsfSdCLwVlVYkNzCca6OOdm_89lwcycjMzDub1FSIy2yeujY14cZuJkgOjP867BWGpzym0UFo1m7eG-Mv53-JTM/s1600/damiana-apigenin.jpg" height="200" width="200" /></a></div>
<b>Apigenin in Damiana, also known as Turnera diffusa, has been shown to kill breast cancer cells (MDA-MB-231) in vitro. </b>Dr. Avelino-Flores and co-workers analyzed anticancer effect of extracts and organic fractions of Damiana plant on five tumor cell lines (SiHa, C-33, Hep G2, MDA-MB-231, and T-47D) and, also on normal human fibroblasts.<br />
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Four organic fractions of methanolic extract exhibited <a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">anticancer activity</a> on MDA-MB-231 cancer cell line. And most active fraction was found to contain arbutin and apigenin. Here is the abstract of this recent study.<br />
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<h3>
Cytotoxic Activity of the Methanolic Extract of Turnera diffusa Willd on Breast Cancer Cells</h3>
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Abstract<br />
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Turnera diffusa Willd, commonly known as Damiana, is employed in traditional medicine as a <b>stimulant, aphrodisiac, and diuretic</b>. Its leaves and stems are used for <b>flavoring </b>and <b>infusion</b>. <b>Damiana is considered to be safe for medicinal use by the FDA.</b><br />
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Pharmacological studies have established the <b>hypoglycemic, antiaromatase, prosexual, estrogenic, antibacterial,</b> and <b>antioxidant activity</b> of T. diffusa.<br />
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The aim of the present study was to evaluate the possible cytotoxic effect of extracts and organic fractions of this plant on five tumor cell lines (<b>SiHa, C-33, Hep G2, MDA-MB-231, and T-47D</b>) and normal human fibroblasts.<br />
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The results show that the methanolic extract (TdM) displayed greater activity on MDA-MB-231 breast cancer cells (with an IC50 of 30.67?µg/mL) than on the other cancer cell lines. Four organic fractions of this extract exhibited activity on this cancer cell line.<br />
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In the most active fraction (F4), two active compounds were isolated, arbutin (1) and apigenin (2).<br />
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<i>This is the first report of a cytotoxic effect by T. diffusa on cancer cells.</i><br />
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<b>The IC50 values suggest that the methanolic extract of T. diffusa has potential as an anticancer therapy.</b><br />
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Original Article;<br />
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Avelino-Flores MD, Cruz-López MD, Jiménez-Montejo FE, Reyes-Leyva J. Cytotoxic Activity of the Methanolic Extract of Turnera diffusa Willd on Breast Cancer Cells. J Med Food. 2014 Oct 9. [Epub ahead of print] PubMed PMID: 25299247.<br />
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http://www.ncbi.nlm.nih.gov/pubmed/25299247<br />
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If you like this post, please share it using below buttonsAnonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-20605226334611640802014-10-07T13:25:00.000-07:002014-11-12T10:52:23.382-08:00Products of Indonesian stingless bee kill human cancer cell lines<br />
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New research published in the “<b>Asian Pacific Journal of Tropical Biomedicine</b>”, showed <b>propolis obtained from Indonesian stingless bees fight cancer cells</b>, in vitro. Dr. Kustiawan PM and co-workers stated the need of further studies to revealing the beneficial effects of bee products such as, <b>propolis, bee pollen and royal jelly</b>.<br />
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Bioactive components found in propolis are <b><a href="http://apigeninresearch.blogspot.com/">apigenin</a>, caffeic acid phenyl ester, kaempferol and naringenin</b> and thus these may cause dying of affect cancer cells, in vitro. Here is the abstract of the article:<br />
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<h3>
<i><u>In vitro cytotoxicity of Indonesian stingless bee products against human cancer cell lines</u></i></h3>
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Propolis, bee pollen and royal jelly are bee products that have been ascribed several medical properties in both traditional medicine and more recently in conventional medicine. <b>It is used to prevent or reduce some diseases or symptoms, such as inflammation, heart disease and cancer</b>.<br />
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<h4>
Aim</h4>
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To screen crude extracts of propolis, bee pollen and honey from four stingless bee species [<i>Trigona incisa (T. incisa)</i>], <i>Timia apicalis, Trigona fusco-balteata</i> and <i>Trigona fuscibasis</i>) native to East Kalimantan, Indonesia for cytotoxic activity against five human cancer cell lines (HepG2, SW620, ChaGo-I, KATO-III and BT474).<br />
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<h4>
Methods</h4>
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All samples were extracted with methanol, and then subpartitioned with n-hexane and ethyl acetate. Each crude extract was screened at 20 µg/mL for in vitro cytotoxicity against the cell lines using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. In addition, four previously shown bioactive components from propolis (apigenin, caffeic acid phenyl ester, kaempferol and naringenin) and two chemotherapeutic drugs (doxorubicin and 5-fluorouracil) were used to evaluate the sensitivity of the cell lines.<br />
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<h4>
Results</h4>
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Overall, crude extracts from propolis and honey had higher cytotoxic activities than bee pollen, but the activity was dependent upon the extraction solvent, bee species and cell line. Propolis extracts from <i>T. incisa</i> and <i>Timia apicalis</i> showed the highest and lowest cytotoxic activity, respectively. Only the HepG2 cell line was broadly sensitive to the honey extracts. For pure compounds, doxorubicin was the most cytotoxic, the four propolis compounds the least, but the ChaGo-I cell line was sensitive to kaempferol at 10 µg/mL and KATO-III was sensitive to kaempferol and apigenin at 10 µg/mL. All pure compounds were effective against the BT474 cell line.<br />
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<h4>
Conclusion</h4>
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<b>Propolis from <i>T. incisa</i> and <i>Trigona fusco-balteata</i> contain an in vitro cytotoxic activity against human cancer cell lines. </b>Further study is required, including the isolation and characterization of the active antiproliferative agent(s).<br />
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<b>Reference:</b><br />
<br />
Kustiawan PM, Puthong S, Arung ET, Chanchao C. <b>In vitro cytotoxicity of Indonesian stingless bee products against human cancer cell lines</b>. <i>Asian Pac J Trop Biomed</i>. 2014 Jul;4(7):549-56.<br />
doi: <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25183275/" rel="nofollow" target="_blank">10.12980/APJTB.4.2014APJTB-2013-0039</a>.<br />
<br />
Antiproliferative activity, Bee product, Cancer cell lines, Cytotoxicity, Ethyl acetate extract, Honey,<br />
Methanol, Propolis, n-Hexane, apigenin, caffeic acid phenyl ester, kaempferol, naringenin<br />
<br />
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25183275/<br />
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Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-73672262193191787452014-10-06T14:10:00.001-07:002014-11-12T10:55:56.416-08:00Combined apigenin and barasertib treatment can manage cetuximab resistance<div style="text-align: justify;">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEicQWlaFpXM7hdfD4wDIOC4TD9vCJk4SCo7kbm95njEVYMpgmX1rK4BKmg-TRrKfvqnTPSced23znJnd2oRg5paA186mPAzNziJ6SPuA-nKaF1rt9t6NcnfdP0evdtb_tNdqIo-AdcTW8M/s1600/hnscc-anatomy.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="apigenin plus barasertib for hnscc therapy" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEicQWlaFpXM7hdfD4wDIOC4TD9vCJk4SCo7kbm95njEVYMpgmX1rK4BKmg-TRrKfvqnTPSced23znJnd2oRg5paA186mPAzNziJ6SPuA-nKaF1rt9t6NcnfdP0evdtb_tNdqIo-AdcTW8M/s1600/hnscc-anatomy.jpg" height="184" title="hnscc treatment with apigenin and barasertib" width="200" /></a></div>
Researchers from Laboratory of Cancer Research and Clinical Oncology, University of Antwerp, Belgium, showed that <b>concomitant <a href="http://apigeninresearch.blogspot.com/p/roles-of-apigenin-in-cancer-prevention.html">apigenin</a> and barasertib treatment may overcome resistance to the cetuximab in head and neck cancers are squamous cell carcinomas (HNSCC). </b></div>
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<a name='more'></a><br /></div>
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<a href="http://www.cancerletters.info/article/S0304-3835(14)00492-3/abstract" rel="nofollow" target="_blank">Overcoming cetuximab resistance in HNSCC: The role of AURKB and DUSP proteins.</a></div>
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Dr. Carolien Boeckx and colleagues performed extensive analysis to reveal <b>mechanisms of cetuximab resistance</b> in head and neck squamous cell carcinoma (HNSCC). Because some tumors develop resistance to cetuximab treatment in time and thus become non-responsive to the treatment</div>
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<h4 style="text-align: justify;">
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Mechanisms of cetuximab resistance</h4>
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Unraveling the underlying mechanisms of cetuximab resistance in head and neck squamous cell carcinoma (HNSCC) is of major importance as many tumors remain non-responsive or become resistant.</div>
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Results</div>
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<i>Their microarray results suggest that "resistant" cells still exhibit RAS-MAPK pathway signaling contributing to drug resistance, as witnessed by low expression of DUSP5 and DUSP6, negative regulators of ERK1/2, and increased expression of AURKB, a key regulator of mitosis.</i></div>
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Conclusion</div>
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They conclude that <b>interrupting the RAS-MAPK pathway by an ERK1/2 inhibitor (apigenin) or an AURKB inhibitor (barasertib) might be a new strategy for overcoming cetuximab resistance</b> in head and neck cancers are squamous cell carcinomas (HNSCC).</div>
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<b>Study Highlights</b></div>
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<ul>
<li><b>Gene expression profiles of cetuximab sensitive and resistant cells</b> were compared.</li>
<li><b>Cetuximab resistant cells still exhibit RAS–MAPK signaling despite EGFR inhibition.</b></li>
<li><b>Resistant cells show up/downregulation of AURKB and DUSP, respectively</b>, as well as features of epithelial-mesenchymal transition (EMT).</li>
<li><b>Concomitant ERK and EGFR inhibition can overcome cetuximab resistance</b>.</li>
<li><b>Strong nuclear AURKB expression</b> by Immunohistochemistry (IHC) was observed in >50% of HNSCC patients.</li>
</ul>
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If you like this post please share so that more people can reach</div>
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<b>Original Article Info</b></div>
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Boeckx C, Op de Beeck K, Wouters A, Deschoolmeester V, Limame R, Zwaenepoel K,</div>
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Specenier P, Pauwels P, Vermorken JB, Peeters M, Van Camp G, Baay M, Lardon F.</div>
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Overcoming cetuximab resistance in HNSCC: The role of AURKB and DUSP proteins.</div>
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Cancer Lett. 2014 Nov 28;354(2):365-77. doi: 10.1016/j.canlet.2014.08.039.</div>
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Articles you may like</div>
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<div style="text-align: start;">
<a href="http://apigeninresearch.blogspot.com/2014/10/apigenin-protects-neuronal-injury.html">Apigenin protects neuronal injury in differentiated PC12 cells</a></div>
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<a href="http://apigeninresearch.blogspot.com/2014/10/beer-contains-apigenin.html" style="text-align: justify;">Beer contains 47 polyphenols including apigenin</a></div>
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Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-15057081989342740352014-10-03T09:17:00.002-07:002014-11-12T10:53:50.257-08:00Apigenin protects neuronal injury in differentiated PC12 cells<div style="text-align: justify;">
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjmY0MBQ95x8AqIKJanAZ3SP3Q2Gzar7DLDBOH7iSX2ATxJqaVC9asOW-FvQVflWeKsyV8J_fA3g0dty1Gl6YyVN8n20RnjIeHffGmFbDlgyhCnc8uhMeIH-tfnAU6LgdbHFM4fwmirzAU/s1600/neuron-apigenin.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjmY0MBQ95x8AqIKJanAZ3SP3Q2Gzar7DLDBOH7iSX2ATxJqaVC9asOW-FvQVflWeKsyV8J_fA3g0dty1Gl6YyVN8n20RnjIeHffGmFbDlgyhCnc8uhMeIH-tfnAU6LgdbHFM4fwmirzAU/s1600/neuron-apigenin.jpg" height="113" width="200" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="background-color: #f1f1f1; color: #888888; font-family: arial, sans-serif; font-size: 13px; line-height: 16px; text-align: left;">Figure adapted from Wikipedia</span></td></tr>
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Recent study, published in the <b>Neurochemical Research</b> at Sep 11, 2014, shows that <b><a href="http://apigeninresearch.blogspot.com/">apigenin</a> may guard neuronal cells by virtue of its protective effects.</b></div>
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Dr. Huizhen Guo and colleagues found that apigenin attenuates oxygen and glucose deprivation/reperfusion (OGD/R) sitimulated neuronal injury mainly via <b>antiapoptotic and antioxidative</b> effects of apigenin.<br />
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<div style="-webkit-text-stroke-width: 0px; color: black; font-family: 'Times New Roman'; font-size: medium; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: auto; text-align: justify; text-indent: 0px; text-transform: none; white-space: normal; widows: auto; word-spacing: 0px;">
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<a href="http://link.springer.com/article/10.1007%2Fs11064-014-1421-0" rel="nofollow" target="_blank">Apigenin Mediated Protection of OGD-Evoked Neuron-Like Injury in Differentiated PC12 Cells</a></h3>
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<b>Ischemic stroke</b> has been confirmed to cause neuronal injury due to its insufficient supply of glucose and oxygen to brain tissue. Previous research has shown that oxidative stress, a result of excessive accumulation of reactive oxygen species (ROS), relates to pathophysiology of ischemic stroke, and causes oxidative damage to biomolecules, eventually leading to programmed cell death. <i>Meanwhile, apigenin has been shown to exhibit antioxidant, anti-inflammatory, anti-cancer properties and neuroprotective action. </i></div>
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Researchers wants to investigate the potential mechanisms underlying the neural protection of apigenin on oxygen and glucose deprivation/reperfusion (OGD/R) induced neuronal injury in differentiated PC12 cells.</div>
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<b>Methods</b></div>
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Cells were pretreated with apigenin for 6 h, and then subjected to OGD for 12 h followed by reperfusion for 24 h. </div>
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They also analyzed cell viability, mitochondrial membrane potential, mRNA levels of antioxidant and detoxifying enzymes, Nrf2 and p53 protein expression, LDH release, apoptosis, intracellular ROS levels.</div>
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<b>Results</b></div>
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The results showed that OGD/R significantly decreased cell viability, mitochondrial membrane potential, mRNA levels of antioxidant and detoxifying enzymes and Nrf2 protein expression, while elevated the release of LDH, cell apoptosis, intracellular ROS level, P53 protein expression and upregulated its downstream genes in PC12 cells. However, apigenin effectively inhibited these undesirable changes induced by OGD/R.</div>
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<b>Conclusion</b></div>
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Their findings demonstrate that this compound attenuates OGD/R induced neuronal injury mainly by virtue of its <b>anti-apoptosis and antioxidative properties</b> via affecting the expression of Nrf2 and P53, and their downstream target gene transcription.</div>
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<span lang="EN-US" style="font-family: "Arial","sans-serif"; font-size: 10.0pt; line-height: 115%; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Arial Unicode MS"; mso-fareast-language: EN-US;">If
you like this post please share so that more people can learn.</span></div>
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<span lang="EN-US" style="font-family: "Arial","sans-serif"; font-size: 10.0pt; line-height: 115%; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Arial Unicode MS"; mso-fareast-language: EN-US;"><br /></span></div>
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<b>Reference</b></div>
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<div style="text-align: justify;">
Guo H, Kong S, Chen W, Dai Z, Lin T, Su J, Li S, Xie Q, Su Z, Xu Y, Lai X.</div>
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Apigenin Mediated Protection of OGD-Evoked Neuron-Like Injury in Differentiated</div>
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PC12 Cells. Neurochem Res. 2014 Sep 11. [Epub ahead of print]</div>
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Related Post</div>
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<a href="http://apigeninresearch.blogspot.com/2014/10/beer-contains-apigenin.html">Beer contains 47 polyphenols including apigenin</a></div>
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Anonymoushttp://www.blogger.com/profile/05224374182855590011noreply@blogger.com0tag:blogger.com,1999:blog-6407359362929739534.post-2261588083618515032014-10-03T08:17:00.004-07:002014-11-12T10:53:16.223-08:00Beer contains 47 polyphenols including apigenin<div style="text-align: justify;">
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEioVL5ZX6c87MCsI2163OTlSmFoDfjcxj_CKK_doM7rkmusQ2iOE6e0i4GcpHkrNeSPOKUiCW9zxcHOQRM92NjsSMOB9uXU1GynYafPpaNj1B99RldPvMFG-qtbEvabia6RlneAMK1-Cuw/s1600/beer-apigenin.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEioVL5ZX6c87MCsI2163OTlSmFoDfjcxj_CKK_doM7rkmusQ2iOE6e0i4GcpHkrNeSPOKUiCW9zxcHOQRM92NjsSMOB9uXU1GynYafPpaNj1B99RldPvMFG-qtbEvabia6RlneAMK1-Cuw/s1600/beer-apigenin.jpg" height="110" width="200" /></a></div>
Researchers from the School of Pharmacy, University of Barcelona, showed that beer contains 47 phenolic compounds and 7 of them was identified for the first time including apigenin.<a name='more'></a></h3>
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<a href="http://www.sciencedirect.com/science/article/pii/S0308814614012205" rel="nofollow" target="_blank">A comprehensive characterisation of beer polyphenols by high resolution mass spectrometry (LC–ESI-LTQ-Orbitrap-MS)</a></div>
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Dr. Paola Quifer-Rada and colleagues say beer is the second most consumed alcoholic beverage in Europe and shown by the European Prospective Investigation into Cancer and Nutrition cohort study to be the main food contributor to hydroxybenzoic acid intake. About 70–80% of the total polyphenol content in beer comes from malt, and the remaining 30–20% from hops.</div>
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<b>Methods</b><br />
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In this work, they used liquid chromatography coupled with an electrospray ionization hybrid linear ion trap quadrupole Orbitrap mass spectrometry technique for an accurate identification of <b>beer polyphenols</b>. </div>
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<b>Results</b><br />
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47 phenolic compounds were identified using high mass accuracy and confirmed by MS2experiments, including simple phenolic acids, hydroxycinnamoylquinics, flavanols, flavonols, flavones, alkylmethoxyphenols, alpha- and iso-alpha-acids, hydroxyphenylacetic acids and prenylflavonoids.<br />
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<b>Conclusion</b><br />
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They stated that as far as we know, 7 of these compounds have been recognised in beer for the first time: <b>feruloylquinic acid, caffeic acid-O-hexoside, coumaric acid-O-hexoside, sinapic acid-O-hexoside, catechin-O-dihexoside, kaempferol-O-hexoside, and apigenin-C-hexoside-pentoside</b>.</div>
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<b>Highlights of the study</b></div>
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Phenolic profile of 4 types of beer has been analyzed by high resolution mass spectrometry.</div>
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Phenolic profile among the four types of beers was very similar.</div>
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47 phenolic compounds were identified, 7 of them are described in beer for the first time.</div>
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<b>Reference </b><br />
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Quifer-Rada P, Vallverdú-Queralt A, Martínez-Huélamo M, Chiva-Blanch G, Jáuregui O, Estruch R, Lamuela-Raventós R. A comprehensive characterisation of beer polyphenols by high resolution mass spectrometry (LC-ESI-LTQ-Orbitrap-MS). Food Chem. 2015 ;169:336-43. doi:10.1016/j.foodchem.2014.07.154<br />
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