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目的观察川芎嗪对心肌缺血再灌注损伤的保护作用及机理。方法采用大鼠冠脉结扎30min后再通20min造成心肌缺血再灌模型。大鼠随机分对照组、缺血组、模型组(缺血再灌组)和川芎嗪保护组。观测心肌细胞膜和线粒体中过氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH·PX)、Ca2 + _ATP酶和K+ ,Na+ _ATP酶活力 ,MDA及心肌钙含量。结果川芎嗪保护组心肌细胞膜SOD、GSH·PX、Ca2 +_ATP酶和Na + ,K +_ATP酶活性较缺血再灌组均有显著性升高(P<0.05或P<0.01) ,丙二醛(MDA)和心肌钙含量却呈显著性降低。线粒体中SOD和GSH·PX活力也呈显著性升高(P<0.05),MDA却为显著性降低。结论川芎嗪对大鼠缺血再灌注损伤心肌有确切保护作用 ,其机理是通过提高对氧自由基的清除及抑制脂质过氧化。
Objective To observe the protective effect and mechanism of tetramethylpyrazine on myocardial ischemia-reperfusion injury. Methods A rat model of myocardial ischemia reperfusion was established after 30 minutes of coronary artery ligation and 20 minutes later. The rats were randomly divided into control group, ischemia group, model group (ischemic reperfusion group) and ligustrazine protection group. The superoxide dismutase (SOD), reduced glutathione (GSH·PX), Ca2 + ATPase and K+, Na+_ATPase activity, MDA and myocardial calcium content were observed in myocardial cell membrane and mitochondria. Results The activities of SOD, GSH·PX, Ca2 + ATPase and Na +, K +_ ATPase in the myocardial cell membrane of the tetramethylpyrazine-protected group were significantly higher than those in the ischemia-reperfusion group (P<0.05 or P<0.01). Aldehyde (MDA) and myocardial calcium content were significantly reduced. The activities of SOD and GSH·PX in mitochondria were also significantly increased (P<0.05), but MDA was significantly decreased. Conclusion Tetramethylpyrazine has a protective effect on ischemia-reperfusion injury of rat myocardium. Its mechanism is to increase the clearance of oxygen free radicals and inhibit lipid peroxidation.