银杏叶提取物对神经元缺糖缺氧/复糖复氧性损伤的作用

目的研究银杏叶提取物(EGB761)对体外培养神经元缺糖缺氧/复糖复氧性损伤的作用,并探讨其作用机制。方法利用体外培养的皮层神经元,通过去除培养液中的葡萄糖和氧气(oxygen andglucose deprivation,OGD)模拟缺血缺氧,恢复糖氧供给模拟再灌流。再灌流时分三组加入不同浓度的EGB761观察其作用。噻唑盐比色法(MTT)测定细胞活性,碘化丙锭(PI)与Hoechst33258双染色观察神经元凋亡,免疫蛋白印迹法测定Bcl-2、Bax蛋白的表达。结果EGB761可减少缺糖缺氧/复糖复氧导致的神经元凋亡,提高因该损伤而下降的MTT值以及Bcl-2蛋白的表达。Bax蛋白在EGB761处理前后均无明显变化。结论EGB761可拮抗缺糖缺氧/复糖复氧导致的神经元凋亡,并且该作用可能与诱导Bcl-2蛋白表达有关。

The effect of ginkgo biloba extract(EGB761) on the injury of neurons after oxygen and glucose deprivation and reoxygenation

Objective To investigate the effect of EGB761 on the injury of neurons after oxygen and glucose deprivation (OGD)and reoxygenation.Methods The ischemic-reperfusion model was established by deprivating both glucose and oxygen.Three different concentrations of EGB761 was added at the beginning of reperfusion.The apoptotic cell number and morphology were measured by propidium iodide(PI)and Hochest33258 double staining.Cell proliferating ability was determined by measuring mitochondrial dehydrogenase activity(MTT assay).Western blotting was used to detect the expression of both Bcl-2 and Bax protein.Results When treating with EGB761,the apoptotic cell number decreased,the reductions of both MTT and expression of Bcl-2 protein induced by OGD/reoxygenation were reversed.Conclusion EGB761 could protect the neurons against OGD/reoxygenation injury,and the mechanism of this effect may be related to alerting Bcl-2/Bax protein expression.