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目的:探讨白藜芦醇预处理对大鼠脑缺血再灌损伤的保护作用及其分子机制。方法:大鼠随机分成假手术组、缺血溶剂组、白藜芦醇预处理组,四动脉阻塞(4-VO)法建立前脑缺血模型,缺血10min/再灌22h,试剂盒检测大鼠海马组织SOD活力及NO、MDA含量变化,RT-PCR法观察GRP78mRNA的表达。结果:缺血溶剂组海马组织SOD活性明显低于假手术组,NO、MDA含量高于假手术组;缺血前白藜芦醇预处理能显著反转缺血诱导的SOD活力和NO、MDA水平变化,脑缺血能明显上调GRP78mRNA水平;白藜芦醇预处理能有效抑制缺血诱导的GRP78表达,与缺血组比有显著性差异。结论:白藜芦醇能通过上调SOD活力,减少NO、MDA的生成来抑制缺血后自由基的生成和积累,继而缓解内质网应激、下调GRP78的表达,减轻缺血性脑组织损伤。
Objective: To investigate the protective effect and mechanism of resveratrol pretreatment on cerebral ischemia reperfusion injury in rats. METHODS: Rats were randomly divided into sham operation group, ischemic solvent group, and resveratrol preconditioning group. Four-VO method was used to establish forebrain ischemia model. Ischemia was performed at 10 min/reperfusion for 22 h. The activity of SOD and the contents of NO and MDA in rat hippocampus were detected. The expression of GRP78 mRNA was observed by RT-PCR. RESULTS: The SOD activity in the hippocampus of the ischemic solvent group was significantly lower than that in the sham operation group. The content of NO and MDA in the ischemic solvent group was higher than that in the sham group. Pretreatment with resveratrol before ischemia significantly reversed the ischemic-induced SOD activity and NO, MDA. Changes in levels, cerebral ischemia can significantly increase the level of GRP78 mRNA; resveratrol pretreatment can effectively inhibit ischemia-induced GRP78 expression, compared with the ischemic group, there is a significant difference. Conclusion: Resveratrol can inhibit the production and accumulation of free radicals after ischemia by up-regulating the activity of SOD, reducing the production of NO and MDA, and then relieve the stress of endoplasmic reticulum, down-regulate the expression of GRP78, and reduce the damage of ischemic brain tissue. .