Objective:To observe the effects of combined extraction of Ginkgo biloba leaves ( EGb ) with edaravone (ED) on brain cell apoptosis and bcl-2/bax expression in rat models with deficiency of Qi and blood stasis after cerebral ischemia reperfusion injury. Methods: Rat models with Qi deficiency and blood stasis were initially developed by starvation,fatigue and intake of high-fat diet, followed by temporary middle cerebral artery occlusion for 2 hours for cerebral ischemic reperfusion injury. After 72-hour therapy of the injury, we observed the effects of single use of EGb and ED as well as combined both agents, respectively, on the brain cell apoptosis and bcl-2/bax expression in the animal models. Results:Simple EGb and ED as well as combined use of the both agents could delay the cell apoptosis, down-regulate the expression of bax but increase bcl-2 except for reduction of the nerve cell injury as compared with the model group( P ＜0. 01 ). Importantly, the effects appeared prominent by combination of the two agents. Conclusion: Combined use of EGb and ED can decrease the expression of bax gene, yet increase bcl-2 expression to inhibit the nerve cell apoptosis and quicken the neurofunctional recovery, suggesting that the two agents play synergistic roles in protecting the brain from cerebral ischemic reperfusion injury.%目的:观察银杏叶提取物(EGb)与依达拉奉(ED)联合应用对气虚血瘀型脑缺血再灌注大鼠脑组织细胞凋亡率及bcl-2/bax表达的影响.方法:采用饥饿、疲劳、高脂饮食等复制大鼠气虚血瘀模型,再用线栓法阻断大脑中动脉2 h,再灌注治疗72 h后,观察EGb、ED及EGb+ED组对气虚血瘀型脑缺血再灌注损伤大鼠脑组织细胞凋亡率及bcl-2/bax表达的影响.结果:与模型组比较,EGb、ED及EGb+ED组均能降低气虚血瘀型脑缺血再灌注损伤大鼠脑组织凋亡细胞数(P<0.01),下调bax基因表达,上调bcl-2基因表达,减轻神经细胞损伤(P<0.01),两药联用变化趋势更明显.结论:银杏叶提取物和依达拉奉能降低气虚血瘀型脑缺血再灌注损伤模型鼠脑组织细胞凋亡基因bax的表达,增加具有神经元保护作用的bcl-2基因表达,从而抑制神经细胞凋亡,加速神经功能的恢复,共同发挥脑保护作用.
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