甲磺酸桂哌齐特对大鼠脑缺血-再灌注损伤的神经保护作用

Neuroprotective effect of cinepazide mesylate on cerebral ischemia-reperfusion injury in rats

目的探讨甲磺酸桂哌齐特对脑缺血-再灌注(I-R)损伤的保护作用及机制。方法 50只雄性SD大鼠用线栓法建立大脑中动脉I-R损伤模型后随机均分为五组:B组为模型对照,C、D和E组分别用甲磺酸桂哌齐特20、40和80mg/kg处理,F组用马来酸桂哌齐特40mg/kg处理;另外取10只雄性SD大鼠作为空白对照(A)组。观察I-R后4、8及22h神经功能缺损、脑含水量、脑指数的变化;I-R损伤24h后测定脑组织超氧化物歧化酶(SOD)、乳酸脱氢酶(LDH)、一氧化氮合酶(NOS)的活力和丙二醛(MDA)、乳酸(LD)的含量。结果与B组比较,D组和E组I-R后8h和22h神经功能缺损评分、脑含水量和脑指数降低(P<0.05);与B组比较,C、D、E、F组I-R脑组织SOD和LDH活性升高、MDA、LD含量和NOS活性降低(P<0.05)。结论甲磺酸桂哌齐特对脑I-R损伤有保护作用;其机制可能与抗自由基损伤、抑制NOS等的升高有关。

Objective To investigate the protective effect of cinepazide mesylate injection（CMI） on cerebral ischemia-reperfusion （I-R） injury and underlying mechanism in rats. Methods The cerebral I-R model was established by ligation of middle cerebral artery in 50 male SD rats, which were equally randomized into 5 groups of B（model control）, C（treated with CMI 20 mg/kg）, D（treated with CMI 40 mg/kg） E（treated with CMI 60 mg/kg） and F（treated with cinepazide maleate 40 mg/kg）. The neurologic deficit score, brain water content and brain index were measured at 4,8 and 22 h after I-R injury. The activities of SOD, LDH, NOS, MDA and LD in brain tissues were measured at 24 h after I-R injury. Results Compared with group B, the neurological deficits, brain water content and brain index were lower in groups of D and E at 8 h and 22 h after I-R injury（P〈0. 05）. The activities of SOD, LDH in brain tissues were higher, but NOS, MDA and LD were lower, in groups of D and E than those in group B（P〈0. 05）. Conclusion CMI has a protective effect on cerebral I-R injury, which may be associated with its interaction with antioxidative stress and inhibition in NOS activity in brain tissues.