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目的:观察脑缺血预处理对脑缺血再灌注损伤大鼠抗氧化酶的影响,探讨脑缺血耐受的作用机制。方法:Wistar大鼠随机分为假手术组、缺血预处理组、缺血再灌注组、缺血耐受组,每组又分为再灌注6h、24h两个时间点。各组于上述各再灌注时间点取脑,制备10%脑匀浆,分光光度法检测脑匀浆中SOD、CAT、GSH-Px、MDA、MPO的水平。结果:与缺血再灌注组比较,缺血耐受组TSOD活力在再灌注6h,24h明显升高;CAT活力有升高的趋势但没有显著性差异,但与缺血预处理组比较,CAT活力在6h,24h明显升高;缺血耐受组MDA、MPO水平在6h或24h显著降低;GSH-px活力在各组间没有显著性变化。结论:脑缺血预处理通过升高抗氧化酶SOD、CAT活力,降低MDA、MPO水平诱导脑缺血耐受,但对GSH-Px水平没有显著影响。
Objective: To observe the effect of cerebral ischemic preconditioning on the antioxidant enzymes in rats with cerebral ischemia-reperfusion injury and to explore the mechanism of cerebral ischemic tolerance. Methods: Wistar rats were randomly divided into sham-operated group, ischemic preconditioning group, ischemia-reperfusion group and ischemic tolerance group. Each group was divided into two groups: reperfusion 6h and 24h. Brain tissue was harvested at each time point of reperfusion, and 10% brain homogenate was prepared. The levels of SOD, CAT, GSH-Px, MDA and MPO in brain homogenate were detected by spectrophotometry. Results: Compared with ischemia reperfusion group, TSOD activity in ischemic tolerance group increased significantly at 6h and 24h after reperfusion; CAT activity increased but there was no significant difference, but compared with ischemic preconditioning group, CAT activity Vitality increased significantly at 6h and 24h, while MDA and MPO levels in ischemic tolerance group decreased significantly at 6h or 24h. GSH-px activity did not change significantly among groups. CONCLUSION: Cerebral ischemia preconditioning induces cerebral ischemic tolerance by elevating the activities of antioxidant enzymes SOD and CAT and decreasing the levels of MDA and MPO, but has no significant effect on the level of GSH-Px.