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目的 探讨大鼠局灶性脑缺血再灌注后受损伤的神经细胞和血管内皮细胞凋亡 ,以及Bcl 2和Bax蛋白表达与再灌注时间的关系。 方法 应用原位末端标记 (TUNEL)技术和免疫组织化学方法 ,分别观察脑缺血再灌注 2h、6h、12h、2 4h、2d、3d、7d、14d和 2 1d等不同时间点神经细胞和血管内皮细胞凋亡数及Bcl 2和Bax蛋白的表达。 结果 1.脑缺血周围区 ,再灌注 2h神经细胞和内皮细胞凋亡开始明显增多 ,12～ 2 4h达高峰 ,之后逐渐减少 ,7～ 14d降至假手术组水平 ;血管内皮细胞凋亡迟于神经元凋亡约 12h。 2 .Bcl 2蛋白表达于缺血再灌注 2h开始逐渐增强 ,12～ 2 4h达高峰 ,之后逐渐下降 ,至 7～ 14d接近假手术组水平 ;3.Bax蛋白表达于缺血再灌注 6h开始逐步增高 ,2 4～ 4 8h达高峰 ,之后逐渐下降 ,至 14d与假手术组已无显著性差异。 4 .Bcl 2表达与细胞凋亡的时相变化基本一致 ,Bax表达时相迟于细胞凋亡。 结论 细胞凋亡是脑缺血再灌注损伤细胞死亡的形式之一 ,血管内皮细胞凋亡迟于神经细胞凋亡 ,Bcl 2和Bax参与细胞凋亡的调节。
Objective To investigate the apoptosis of nerve cells and vascular endothelial cells after focal cerebral ischemia-reperfusion in rats and the relationship between the expression of Bcl-2 and Bax and the reperfusion time. Methods TUNEL and immunohistochemical methods were used to observe the changes of neural cells and blood vessels at different time points after 2h, 6h, 12h, 24h, 2d, 3d, 7d, 14d and 21d after cerebral ischemia / reperfusion Endothelial cell apoptosis and expression of Bcl 2 and Bax proteins. Results 1. Peripheral area of cerebral ischemia, the apoptosis of neurons and endothelial cells began to increase at 2h after reperfusion, reached the peak at 12 ~ 24h, then decreased gradually and dropped to the level of sham operation 7 ~ 14d. The apoptosis of vascular endothelial cells was delayed Neuronal apoptosis for about 12h. The expression of Bcl-2 protein gradually increased at 2h after ischemia-reperfusion, reaching the peak at 12 ~ 24h, then gradually decreased, reaching the level of sham-operated group at 7 ~ 14d; 3. The expression of Bax protein gradually began at 6h after ischemia-reperfusion Increased from 24 to 48 h after reaching the peak, then gradually decreased to 14d and sham operation group no significant difference. The change of Bcl 2 expression was consistent with that of apoptosis, and the expression of Bax was later than that of apoptosis. Conclusion Apoptosis is one of the forms of cell death in cerebral ischemia-reperfusion injury. Vascular endothelial cell apoptosis is later than that of neuronal apoptosis, and Bcl 2 and Bax are involved in the regulation of apoptosis.