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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。
OBJECTIVE To study the effects of Ginkgo biloba extract (EGB761) on hypoxia-hypoxia-reoxygenation-reoxygenation injury of neurons cultured in vitro, and to explore its mechanism of action. Methods The cortical neurons cultured in vitro were used to simulate ischemia and hypoxia by removing glucose and oxygen (OGD) in the culture medium, and the sugar and oxygen supply was restored to simulate reperfusion. After reperfusion, three groups of EGB761 were added to observe their effects. The cell viability was measured by thiazolyle colorimetry (MTT), neuron apoptosis was observed by propidium iodide (PI) and Hoechst 33258 staining, and the expression of Bcl-2 and Bax protein was detected by Western blotting. Results EGB761 reduced the neuronal apoptosis induced by hypoxia/hypoxia/resurrection glucose and reoxygenation, and increased the MTT value and the expression of Bcl-2 protein. There was no significant change in Bax protein before and after treatment with EGB761. Conclusion EGB761 can antagonize the neuronal apoptosis induced by hypoxia/hypoxia/resurrection of glucose, and this effect may be related to the induction of Bcl-2 protein expression.