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目的 探讨 Ｂｃｌ２ 及 Ｆａｓ 蛋白在大鼠脑缺血再灌注损伤中的表达及与缺血性凋亡的关系。方法 采用免疫组化方法观察 Ｂｃｌ２ 及 Ｆａｓ 蛋白在脑缺血再灌注后随时间延长动态变化并用图像分析测定二者的免疫强度。结果 脑缺血再灌注后 Ｂｃｌ２、 Ｆａｓ 表达。 Ｂｃｌ２ 蛋白表达于再灌注 ３ｈ 达高峰，再灌注 ６ｈ 其表达呈下降趋势，再灌注 ２４ｈ 仅少数细胞阳性表达。 Ｆａｓ 蛋白表达于再灌注 ６ｈ 达高峰，对缺血较敏感的海马大锥体细胞亦有表达，再灌注 ２４ｈ 其表达减少。结论 Ｆａｓ 蛋白表达介导了脑缺血后细胞凋亡的发生，并可能参与了迟发性神经元死亡。 Ｂｃｌ２ 表达与神经元存活密切相关，在神经元缺血敏感性方面起重要作用，对神经元起保护作用。
Objective To investigate the expression of Bcl2 and Fas proteins in cerebral ischemia-reperfusion injury in rats and its relationship with ischemic apoptosis. Methods Immunohistochemistry was used to observe the dynamic changes of Bcl2 and Fas proteins with time after cerebral ischemia and reperfusion, and their immunostaining intensity was measured by image analysis. Results After cerebral ischemia-reperfusion Bcl 2, Fas expression. The expression of Bcl2 protein peaked at 3h after reperfusion, and then decreased at 6h after reperfusion. Only a few cells were positive after reperfusion for 24h. The expression of Fas protein peaked at 6h after reperfusion, and also expressed in the hippocampal pyramidal cells sensitive to ischemia. The expression of Fas protein decreased at 24h after reperfusion. Conclusion Fas protein expression mediates the occurrence of apoptosis after cerebral ischemia and may be involved in the delayed neuronal death. Bcl 2 expression is closely related to neuronal survival, plays an important role in neuronal ischemic sensitivity, play a protective role on neurons.