白藜芦醇对脑梗死大鼠的脑保护作用及抗氧化机制研究

The neuroprotective effects and anti-oxidation mechanisms of polydatin in rat cerebral ischemia

目的 探讨白藜芦醇的脑保护作用及机制研究。方法 用改良线栓法制备SD大鼠大脑中动脉闭塞(MCAO)模型。实验动物随机分为白藜芦醇组,溶剂对照组和假手术组。实验1检测白藜芦醇脑保护作用:比较各组神经功能缺损评分,脑梗死体积和患侧脑水肿。实验2检测白藜芦醇对脑梗死的抗氧化作用,采用试剂盒检测超氧化物歧化酶(SOD),过氧化氢酶(CAT),丙二醛(MDA)的变化,RTqPCR和Western blot检测核转录因子NF-E2相关因子(Nrf-2)、血红素氧合酶-1(HO-1)基因和蛋白表达变化。结果 实验1:白藜芦醇减轻神经功能缺损,减小脑梗死体积,减轻患侧脑水肿;试验2:白藜芦醇提高SOD和CAT水平,升高Nrf-2、HO-1表达,减少MDA水平。结论①白藜芦醇具有脑保护作用;②白藜芦醇通过调节SOD,CAT,MDA,Nrf-2、HO-1的表达起到抗氧化作用。

Objective To study the protective effects of polydatin on cerebral ischemia injury and the potential mechanisms.Methods The model of middle cerebral artery occlusion(MCAO) in SD rats was established by modified thread embolization method.In experiment 1,rats were randomly divided into three groups:vehicle group,sham group and polydatin group.The brain neurological deficits,infarct volume and water content were measured.In experiment 2,rats were reanesthetized and killed at 24 h after surgery.The effect on SOD,CAT,MDA were detected by reagent test kit,Nrf-2 and HO-1 were detected by RT-qPCR and Western blot.Results In experiment 1,polydatin significantly suppressed edema,alleviated neurological deficit and decreased infarct volume.In experiment 2,polydatin obviously elevated the level of SOD and CAT,the expression of Nrf-2 and HO-1,reduced the level of MDA.Conclusion Polydatin protected the brain from the damage caused by pMCAO.SOD,CAT,MDA,Nrf-2 and HO-1 are involved in the Polydatin ’ s anti-oxidation effect in cerebral ischemia.