左卡尼汀对脑缺血再灌注损伤的抗氧化作用及其机制研究

目的：观察左卡尼汀对脑缺血再灌注损伤的保护作用，探讨其作用机制。方法：健康雄性Wistar大鼠40只，随机分成4组：假手术组、生理盐水对照组、左卡尼汀100mg／kg治疗组及左卡尼汀200mg／kg治疗组，每组10只。采用线栓法制备大脑中动脉缺血再灌注模型，缺血2h，再灌注24h，观察左卡尼汀对脑组织丙二醛（MDA）、超氧化物歧化酶（SOD）含量的影响，HE染色观察大鼠脑组织的病理改变。结果：左卡尼汀可明显减少MDA的含量，升高SOD活性，同生理盐水对照组相比，P〈0．01。结论：左卡尼汀对脑缺血再灌注损伤有保护作用，与提高脑组织中抗氧化酶活性、抑制氧自由基产生及脂质过氧化反应有关。

The antioxidant effect of levocarnitine in focal cerebral ischemia-reperfusion induced injury rats and its mechanism

Objective：To investigate the protective effects of levocarnitine on cerebral ischemia-reperfusion（I/R） injury in rats and analyze the mechanism of action of levocarnitine in preventing and treating ischemie cerebrovaseular disease. Methods;Forty healthy male wistar rats were randomly alloeated into four groups：sham operation group, saline-eontroled group,treated with 100 mg/kg of levocarnitine group and treated with 200 mg/kg of levoearnitine group,each of ten rats. The models of the focal cerebral I/R rats were made by the middle cerebral artery occlusion （MCAO）except sham-operation group. After ischemia for 2 h and reperfusion for 24 h ,malondialdehyde（MDA）levels and superoxide dismutase （SOD） activity were measured in the cerebral tissues. The pathological feature of cerebral tissue was detected by HE staining. Results . Levocarnitine injection significantly suppressed MDA levels,prevented redUction of SOD activity in comparison with the saline-eontroled group （P〈0. 01）. Conclusion;The results demonstrated that levocarnitine has a potent neuroprotective effect against cerebral I/R induced injury to enhance the ac tivity of the antioxidant system and decrease the incidence of free radical induced lipid peroxidation in rat brain.