川芎嗪对大鼠心肌缺血再灌注损伤保护作用的研究

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30 min后再通20 min 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。

Protective effects of liqustrazin on myocardial ischemia-reperfusion injury in rats

Aim The effect of liqustrazin on myocardial ischemia leperfusion injury in rats was observd. Methods The rat model of myocardial ischemia tepeifusion was established by ligating coro-nary artery. The rats were randomly divided in the control, model and liqustrazin treated groups. The activities of SOD, GSH · PX, Ca²⁺-ATPase, K⁺, Na⁺ ATPase and contents of MDA and Ca²⁺ were observed respectively. Results In the liqustrazin treated group as compared with those of the model, the activities of SOD, GSH · PX, Ca²⁺ ATPase, K⁺, Na⁺ -ATPase in the myocardial membrane increased significantly (P ＜0.01 or P ＜0.05) w hile contents of MDA and Ca²⁺ decreased (P ＜0.01) significantly. Activities of SOD and GSH · PX in the mitochondria was also increased (P ＜0.01) and MDA content decreased (P ＜0.01). Conclusions Liqustrazin has notable protective effects on myocardial-ischemia leperfusion injury in rats, which is due to its scarenging oxygen free radicals and anti ipid peroxydation reaction.