摘要
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。
Aim The effect of liqustrazin on myocardial ischemia_reperfusion injury in rats was observd . Methods The rat model of myocardial ischemia_reperfusion was established by ligating coronary 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),while 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_reperfusion injury in rats, which is due to its scarenging oxygen free radicals and anti_lipid peroxydation reaction.
