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目的 研究不同浓度银杏叶提取物 (GBE)对大鼠脑缺血再灌注损伤皮质内自由基动态平衡的影响。方法 将 119只Wistar大鼠随机分为 17组 ,假手术组 7只 ,缺血组—缺血 3h组 ,缺血 3h分别再灌注 1h、2h、3h组各 7只 ;治疗组 (即在缺血前 30分钟给予GBE 5mg/kg、10mg/kg、15mg/kg ,腹腔给药 )—缺血 3h ,但缺血 3h分别灌注 1h、2h、3h组各 7只。动物模型参照Zivin的大脑中动脉线栓模型并加以改进。结果 比较缺血组和治疗组 ,可见给予GBE后能明显减少丙二醛 (MDA)的产生 ,增加的超氧化物歧化酶 (superoxidedismutase ,SOD) ,SOD的测定采用黄嘌呤法 ,谷胱甘肽过氧化物酶 (glutathioneperoxi dase ,GSH PX)生成和释放 ,5mg/kg组与 10mg/kg、15mg/kg组间有显著差别 ,而后二者间无显著差别。结论 血小板活化因子拮抗剂GBE可通过增强SOD和GSH PX的合成、释放 ,降低MDA的合成、保护缺血的神经元 ,且与用药剂量有关。
Objective To study the effects of different concentrations of ginkgo biloba extract (GBE) on the dynamic balance of free radicals in cerebral cortex after cerebral ischemia-reperfusion injury in rats. Methods One hundred and nineteen Wistar rats were randomly divided into 17 groups, sham-operation group (7 rats), ischemia group (3h), ischemia group GBE 5mg / kg, 10mg / kg, 15mg / kg given 30 minutes before the blood supply - ischemia 3h, but ischemia 3h perfusion 1h, 2h, 3h group 7 each. The animal model is referenced to Zivin’s model of middle cerebral artery occlusion and improved. Results Compared with the ischemic group and the treatment group, it was found that the administration of GBE significantly reduced the production of malondialdehyde (MDA), and the increased superoxide dismutase (SOD) and superoxide dismutase (SOD) were detected by xanthine method, glutathione Peroxidase (GSH PX) production and release, 5mg / kg group and 10mg / kg, 15mg / kg group was significantly different, and then there was no significant difference between the two. Conclusion The platelet-activating factor antagonist GBE can protect the ischemic neurons by increasing the synthesis and release of SOD and GSH PX, and decreasing the synthesis of MDA.