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葛根素对大鼠心肌缺血再灌注损伤的保护作用及抗氧化应激机制的探讨
引用本文:贾长海,秦亚玲,任斌蓉. 葛根素对大鼠心肌缺血再灌注损伤的保护作用及抗氧化应激机制的探讨[J]. 辽宁中医学院学报, 2010, 0(11): 230-232
作者姓名:贾长海  秦亚玲  任斌蓉
作者单位:[1]成都市第一人民医院急诊科,四川成都610000 [2]四川大学华西青羊校区,四川成都610091
摘    要:目的:探讨葛根素对大鼠心肌缺血再灌注损伤的保护作用(Myocardial Ischemia-reperfusion Injury,MIRI)及抗氧化应激机制。方法:大鼠心肌缺血30min后再灌注180min造成大鼠心肌缺血再灌注损伤模型(灌注24 h,用于测定心肌梗死面积)。实验组和对照组分别给予葛根素和生理盐水。收集大鼠心脏,观察大鼠心肌缺血区的心肌细胞凋亡情况;收集血清测定其抗氧化应激的指标。结果:与模型组相比,葛根素剂量依赖性的减少了MIRI大鼠的心肌细胞凋亡、心梗面积和血清中丙二醛的含量,增加了血清中超氧化物歧化酶、谷胱甘肽过氧化物酶的活性和谷胱甘肽的含量。结论:葛根素对MIRI大鼠具有抗氧化应激的作用,它能够剂量依赖性的减少心肌细胞凋亡,最终减少心肌梗死面积。

关 键 词:葛根素  心肌缺血再灌注损伤  抗氧化应激  心肌细胞凋亡

Puerarin Protects Heart Against Oxidative Stress Induced by Acute Myocardial Ischemia-Reperfusion Injury in Rats
JIA Chang-hai,QIN Ya-ling,REN Bin-rong. Puerarin Protects Heart Against Oxidative Stress Induced by Acute Myocardial Ischemia-Reperfusion Injury in Rats[J]. Journal of Liaoning College of Traditional Chinese Medicine, 2010, 0(11): 230-232
Authors:JIA Chang-hai  QIN Ya-ling  REN Bin-rong
Affiliation:1.Emergency Department,Chengdu First People's Hospital,Chengdu 610000,Sichuan,China;2.Huaxi Qingyang Campus,Sichuan University,Chengdu 610091,Sichuan,China)
Abstract:Objective:To investigate the protective mechanism of puerarin on acute Myocardial Ischemia-reperfusion Injury(MIRI)rats,and to explain the antioxidative mechanism involved.Methods:MIRI rat model was induced by ischemia for 30 min and then reperfusion for 180 min.At the end of the 3h reperfusion period(or 24h for infarct size),we measured the myocardial infarct size,myocardial apoptosis and the activities of antioxidative enzymes.Results:Puerarin reduced infarct size,myocardial apoptosis and the serum level of malondialdehyde,increased the activities of superoxide dismutase and glutathione-peroxidase activities and serum level of glutathione.Conclusion:Puerarin exerts significant cardioprotective effects against MIRI in rats,likely through its antioxidation and antilipid peroxidative properties.
Keywords:puerarin  myocardial ischemia-reperfusion injury  oxidative stress  myocardial apoptosis
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