氧化苦参碱对局灶性脑缺血大鼠氧化应激反应的干预作用

目的：观察氧化苦参碱(OMT)对局灶性脑缺血大鼠的干预作用，并探讨其干预氧化应激反应的机制。方法：Wistar大鼠随机分为假手术组、模型组、阳性药组、OMT1（35 mg/kg）组、OMT2（70 mg/kg）组和OMT3（105 mg/kg）组，每组10只。各组动物在造模前5 d预防性腹腔注射给药或生理盐水。利用线栓法制备大鼠大脑中动脉阻塞（MCAO）模型。术后24 h对大鼠进行神经功能学评分，TTC染色计算脑梗死体积比，并通过HE染色及血清中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活性以及丙二醛(MDA)的血清含量检测观察OMT对大鼠脑缺血损伤的影响。结果: 与模型组比较，OMT各组大鼠神经学评分明显降低(P<0.05或P<0.01)；缺血脑组织和细胞的水肿程度减轻，梗死灶减少，脑组织和细胞的形态维持正常，脑梗死体积比降低(P<0.05或P<0.01)；且脑缺血大鼠外周血清中SOD、CAT和GSH-Px的活性增加(P<0.05或P<0.01)，MDA的含量降低(P<0.05或P<0.01)，具有明显的量效关系。结论：OMT可以通过影响脑缺血大鼠的氧化应激反应干预脑缺血损伤。

Interventional effects of oxymatrine on oxidative stress response of focal cerebral ischemia in rats

Objective To investigate the interventional effect of oxymatrine (OMT) on focal cerebral ischemia and explore the mechanism of its intervention on oxidative stress response.Methods The Wistar rats were randomly divided into sham operation group,model group,positive drug group,OMT1(35 mg·kg-1) group,OMT2(70 mg·kg-1) group and OMT3(105 mg·kg-1) group(n=10).The drug was continuously administrated 5 d before the surgery of middle cerebral artery occlusion(MCAO) was carried out.The neurological score was recorded 24 h after operation and the morphological changes of ischemic brain tissue were observed by HE staining.The interventional effects of OMT on oxidative stress of cerebral ischemic rats were investigated by measuring the activities of superoxide dismutase(SOD),catalase(CAT) and glutathione-SH peroxydase(GSH-Px) and the content of malondialdehyde(MDA) in peripheral serum.Results Compared with model group,the neurological scores of rats in OMT groups were significantly decreased(P<0.05 or P<0.01),the morphological characteristics of ischemic brain tissue were maintained and the damage of tissue was alleviated with a certain degree;the activities of SOD,CAT and GSH-Px were increased(P<0.05 or P<0.01) and the contents of MDA reduced(P<0.05 or P<0.01) with a dose-effect relationship.Conclusion OMT can intervene the focal cerebral ischemic injury by influencing the oxidative stress respone in rats with cerebral ischemic injury.