کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5846233 | 1128462 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Resveratrol attenuates methylglyoxal-induced mitochondrial dysfunction and apoptosis by Sestrin2 induction
ترجمه فارسی عنوان
رسکوراترول باعث اختلال در عملکرد میتوکندری ناشی از متیل گلیکسال و آپوپتوز توسط القاء سسترین 2 می شود
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کلمات کلیدی
AGEsSESNNQORh123Sestrin2PRXRAGEHeme oxygenase-1GCLsirtuinSIRTAMPKDCFH-DAHO-1GSHALTNrf22′,7′-dichlorofluorescein diacetate - 2 '، 7'-dichlorofluorescein diacetate3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyl tetrazolium bromideAMP-activated protein kinase - AMP-پروتئین کیناز فعال شده استMTT - MTTSmall interfering RNA - RNA تداخل کوچکsiRNA - siRNAAST - آسپارتات ترانس آمینازAspartate aminotransferase - آسپارتات ترانس آمیناز یا AST Alanine aminotransferase - آلانین آمینوترانسفرازMitochondrial dysfunction - اختلال در عملکرد میتوکندریOxidative stress - تنش اکسیداتیوSestrin - خواهرResveratrol - رسوراترولRhodamine123 - رودامین 123NF-E2-related factor-2 - فاکتور 2 مربوط به NF-E2glutamate cysteine ligase - لیگاز سیتئین گلوتاماتMethylglyoxal - متیل گلی اکسالAdvanced glycation end products - محصولات نهایی پیشرفته گلیساسیونPeroxiredoxin - پروکسی ردوکسینGlutathione - گلوتاتیونReactive oxygen species - گونههای فعال اکسیژنReceptor for advanced glycation end products - گیرنده برای محصولات پیشرفته glycation پایان
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی
Methylglyoxal is found in high levels in the blood and other tissues of diabetic patients and exerts deleterious effects on cells and tissues. Previously, we reported that resveratrol, a polyphenol in grapes, induced the expression of Sestrin2 (SESN2), a novel antioxidant protein, and inhibited hepatic lipogenesis. This study investigated whether resveratrol protects cells from the methylglyoxal-induced toxicity via SESN2 induction. Methylglyoxal significantly induced cell death in HepG2 cells. However, cells pretreated with resveratrol were rescued from methylglyoxal-induced apoptosis. Resveratrol attenuated glutathione (GSH) depletion and ROS production promoted by methylglyoxal. Moreover, mitochondrial damage was observed by methylglyoxal treatment, but resveratrol restored mitochondrial function, as evidenced by the observed lack of mitochondrial permeability transition and increased ADP/ATP ratio. Resveratrol treatment inhibited SESN2 depletion elicited by methylglyoxal. SESN2 overexpression repressed methylglyoxal-induced mitochondrial dysfunction and apoptosis. Likewise, rotenone-induced cytotoxicity was not observed in SESN2 overexpressed cells. Furthermore, siRNA knockdown of SESN2 reduced the ability of resveratrol to prevent methylglyoxal-induced mitochondrial permeability transition. In addition, when mice were exposed to methylglyoxal after infection of Ad-SESN2, the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and GSH depletion by methylglyoxal in liver was reduced in Ad-SESN2 infected mice. Our results demonstrated that resveratrol is capable of protecting cells from methylglyoxal-induced mitochondrial dysfunction and oxidative stress via SESN2 induction.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology and Applied Pharmacology - Volume 280, Issue 2, 15 October 2014, Pages 314-322
Journal: Toxicology and Applied Pharmacology - Volume 280, Issue 2, 15 October 2014, Pages 314-322
نویسندگان
Kyuhwa Seo, Suho Seo, Jae Yun Han, Sung Hwan Ki, Sang Mi Shin,