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目的 探讨脑缺血再灌流损伤时神经细胞凋亡及其调控基因 bcl- 2的作用。方法 采用大鼠大脑中动脉 (MCA)阻断模型阻断血流 2小时后再灌注 ,分别在不同再灌注时间将大鼠断头取脑 ,连续切片分别作 HE、TUNEL染色及 bcl- 2蛋白免疫组化染色。结果 (1) MCA阻断后脑缺血周边区部分神经细胞发生凋亡 ,随着再灌注时间的延长 ,一定时程内凋亡细胞逐渐增多 ,2 4小时达高峰 ,各组之间及与假手术组之间差异显著 (P<0 .0 1)。 (2 )凋亡抑制基因 bcl- 2在再灌注早期 (6小时 )即达高峰 ,各组大鼠 bcl- 2表达亦存在显著差异 (P<0 .0 1)。 (3)神经细胞凋亡的出现与 bcl- 2表达在一定时程内呈直线负相关 (r=- 0 .747,P<0 .0 1)。结论 脑缺血再灌流损伤时 ,神经细胞凋亡起着重要作用 ,这种作用与 bcl- 2的表达等密切相关。
Objective To investigate the effects of bcl-2 on neuronal apoptosis and cerebral ischemia-reperfusion injury. Methods The MCA occlusion model was used to block the blood flow for 2 hours and then reperfusion. The rats were decapitated and reperfused at different time points. The sections were stained with HE, TUNEL and bcl-2 protein respectively Immunohistochemistry. Results (1) Apoptosis of some nerve cells in the peripheral area of MCAO occlusion occurred after MCA occlusion. With the prolongation of reperfusion time, apoptotic cells gradually increased in a certain period of time, reached the peak at 24 hours, The difference between the operation group was significant (P <0.01). (2) The apoptosis-inhibiting gene bcl-2 peaked in the early reperfusion period (6 hours), the expression of bcl-2 in each group also had significant difference (P <0.01). (3) The appearance of neuronal apoptosis was negatively correlated with the expression of bcl-2 in a certain time course (r = - 0.747, P <0.01). Conclusion Neuronal apoptosis plays an important role in cerebral ischemia-reperfusion injury, which is closely related to the expression of bcl-2.