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葛根素预处理对缺血再灌注心肌脂质过氧化与内质网应激的影响
引用本文:冯毅,马亚飞,张林波,王晓峰,魏丽娟. 葛根素预处理对缺血再灌注心肌脂质过氧化与内质网应激的影响[J]. 现代保健, 2014, 0(8): 11-12
作者姓名:冯毅  马亚飞  张林波  王晓峰  魏丽娟
作者单位:河南科技大学附属第一医院,河南洛阳471000
摘    要:目的:观察葛根素预处理对缺血再灌注(I/R)大鼠心肌内质网应激(ERS)与细胞凋亡的影响。方法:采用随机数字表法将24只大鼠分为假手术组(SH组),缺血再灌注组(I/R组),葛根素预处理组(PU组)三组,每组8只。实验结束测定心肌丙二醛(MDA)和超氧化物歧化酶(SOD)的含量以及GRP78 mRNA、CRT mRNA的表达。结果:与SH组比较,其余两组GRP78 mRNA与CRT mRNA表达、心肌MDA含量均明显增加,而心肌SOD水平明显降低(P〈0.05)。与I/R组比较,PU组GRP78 mRNA与CRT mRNA表达、心肌MDA含量均降低,且心肌SOD水平明显增加(P〈0.05)。结论:葛根素预处理可能通过减轻心肌脂质过氧化反应,抑制I/R导致的过度ERS而发挥心肌保护作用。

关 键 词:葛根素  缺血再灌注  内质网应激  脂质过氧化

Effects of Puerarin on Ischemia/Reperfusion Myocardial Lipid Peroxidation and Endoplasmic Reticulum Stress in Rats
Affiliation:FENG Yi, MA Ya-fei, ZHANG Lin-bo, et ai. (First-author's address: The First Affdiated Hospital of Henan University of Science and Technology, Luoyang 471000, China)
Abstract:Objective:To investigate the effect of endoplasmic reticulum stress(ERS)and apoptosis during myocardium ischemia reperfusion with Puerarin preconditioning in rats.Method:Twenty-four Male SD rats were divided randomly into three groups(n=8),sham operation group(SH),ischemia reperfusion group(IR)and Puerarin preconditioning group(PU).The myocardial injury of rats ware produced by the ligation of left coronary artery for 30 min followed by 120 min reperfusion.The Malondialdehyde(MDA),Superoxide Dismutase(SOD),glucose-regulated protein 78(GRP78)mRNA and calreticulin(CRT)mRNA were measured at the end of reperfusion.Result:Compared with the SH group,the expressions of MDA,GRP78 and CRT mRNA of the other two groups increased significantly(P〈0.05),while the level of SOD decreased markedly(P〈0.05). Compared with the I/R group,the level of MDA,GRP78 and CRT mRNA were significantly lower in PU group(P〈0.05),while the level of SOD increased significantly(P〈0.05). Conclusion:Preconditioning with puerarin may regulate ERS response and inhibit excessive ERS by reducing lipid peroxidation during myocardial ischemia reperfusion.
Keywords:Puerarin  Ischemia-reperfusion  Endoplasmic reticulum stress  Lipid peroxidation
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