کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10752536 | 1050328 | 2015 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Resveratrol induces cell apoptosis in adipocytes via AMPK activation
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Resveratrol is identified as polyphenolic compound with anti-inflammatory, antioxidant, anti-insulin resistance characteristics. Moreover, resveratrol exerts pro-apoptotic effects in varieties of cancer cell lines. However, effects and mechanisms of resveratrol on the regulation of adipocytes apoptosis remain largely unknown. In this study, we found that resveratrol treatment could induce cell apoptosis in murine 3T3-L1 adipocytes. Furthermore, resveratrol activated the mitochondrial apoptotic signaling pathway with the decrease in the mitochondrial membrane potential (MMP), and the activation of caspase 3. Mechanistically, we found that phosphorylation level of AMP-activated protein kinase α (AMPKα) was elevated, accompany with reduced level of phosphorylation of protein kinase B (AKT) when cells were exposed to resveratrol. By using small interfering RNAs of AMPKα and specific inhibitor for p-AKT, it was shown that activation of AMPKα could inhibit downstream of p-AKT, consequently activating mitochondrion-mediated apoptotic pathway. Additionally, we observed similar pro-apoptotic effects of Res on mouse primary adipocytes. Our findings clarified the apoptotic effects and underlying mechanisms of resveratrol in adipocytes, suggesting its potential therapeutic application in the treatment or prevention of obesity and related metabolic symptoms.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 457, Issue 4, 20 February 2015, Pages 608-613
Journal: Biochemical and Biophysical Research Communications - Volume 457, Issue 4, 20 February 2015, Pages 608-613
نویسندگان
Sifan Chen, Niman Zhou, Zili Zhang, Wenxue Li, Wei Zhu,