临床医学论文-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.doc

临床医学论文-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
【摘要】  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100 mg/kg治疗组及左卡尼汀200 mg/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2 h，再灌注24 h，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，。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。
【关键词】  左卡尼汀;脑缺血再灌注;丙二醛;超氧化物歧化酶
　　Abstract Objective：：Forty healthy male wistar rats were randomly allocated into four groups：sham operation group，salinecontroled group，treated with 100 mg/kg of levocarnitine group and treated with 200 mg/kg of levocarnitine group，each of ten models of the focal cerebral I/R rats were made by the middle cerebral artery occlusion(MCAO)except shamoperation ischemia for 2 h and reperfusion for 24 h，：Levocarnitine injection significantly suppressed MDA levels，prevented reduction of SOD activity in comparison with the salinecontroled group(P<).Conclusion：The results demonstrated that levocarnitine has a potent neuroprotective effect against cerebral I/R induced injury to enhance the activity of the antioxidant system and decrease the incidence of free radicalinduced lipid peroxidation in rat brain.
　　Key words levocarnitine;cerebral ischemia reperfusion;malondialdehyde;superoxide dismutase
　　本实验通过观察左卡尼汀对大鼠脑缺血再灌注脑组织超氧化物歧化酶(SOD)和丙二醛(MDA)水平的影响，探讨其对脑缺血再灌注损伤的保护作用及可能的作用机制，为临床应用左卡尼汀治疗脑梗死提供理论依据。