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银杏叶提取物对AGEs诱导心肌细胞内质网应激的影响
引用本文:沈明志,徐勇,李榕彬,欧书林,王昌,穆洋.银杏叶提取物对AGEs诱导心肌细胞内质网应激的影响[J].现代生物医学进展,2013,13(14):2633-2635,2793.
作者姓名:沈明志  徐勇  李榕彬  欧书林  王昌  穆洋
作者单位:解放军总医院海南分院心内科 海南三亚572013
摘    要:目的:探索银杏叶提取物对晚期糖基化终产物(AGEs)作用下心肌细胞损伤以及内质网应激标记性分子GRP 78和CHOP的影响。方法:原代培养SD大鼠乳鼠心肌细胞,随机分为对照组、AGEs组、AGEs+银杏叶提取物组。MTT法检测心肌细胞存活率,Western blot法检测GRP 78和CHOP蛋白表达水平。结果:与对照组比较,AGEs组48、72 h时心肌细胞存活率降低;与AGEs组比较,银杏叶提取物处理增加心肌细胞存活率。与对照组比较,AGEs组GRP 78和CHOP蛋白表达水平显著升高;与AGEs组比较,银杏叶提取物组GRP 78和CHOP表达水平显著下调。结论:银杏叶提取物能够抑制AGEs诱导的心肌细胞损伤,其机制可能与拮抗GRP 78和CHOP的表达,减轻内质网应激有关。

关 键 词:银杏叶提取物  晚期糖基化终产物  心肌细胞  损伤  内质网应激

Effects of EGB on AGEs-induced Endoplasmic Reticulum Stress in Cardiomyocytes
SHEN Ming-zhi,XU Yong,LI Rong-bin,OU Shu-lin,WANG Chang,MU Yang.Effects of EGB on AGEs-induced Endoplasmic Reticulum Stress in Cardiomyocytes[J].Progress in Modern Biomedicine,2013,13(14):2633-2635,2793.
Authors:SHEN Ming-zhi  XU Yong  LI Rong-bin  OU Shu-lin  WANG Chang  MU Yang
Institution:(Department of Cardiology,Hainan Branch of PLA General Hospital,Sanya,Hainan,572013,China)
Abstract:Objective: To investigate the effects of EGB on advanced glycosylation end products(AGEs)-induced cardiomyocyte injury and expressions of endoplasmic reticulum stress(ERS) markers such as GRP 78 and CHOP.Methods: Cultured neonatal rat cardiomyocytes were randomly divided into control group,AGEs group and AGEs+EGB group.MTT assay was used to measure cell viability.Protein levels of GRP 78 and CHOP were surveyed by western blot assay.Results: Compared with control group,Tm group(48,72 h) resulted in a significant decrease in cell viability.Presence of EGB markedly improved cell viability,compared with AGEs group.Exposure of cardiomyocytes to AGEs resulted in significant upregulations of GRP 78 and CHOP.Co-treatment of EGB and AGEs led to attenuation of GRP 78 and CHOP.Conclusion: These findings demonstrate that EGB protects cardiomyocytes against AGEs-induced cardiomyocyte injury.It may be associated with attenuation of endoplasmic reticulum stress.
Keywords:EGB  Advanced glycosylation end products  Cardiomyocytes  Injury  Endoplasmic reticulum stress
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