缺氧缺血性脑损伤大鼠脑内bcl-2基因表达与细胞凋亡的关系

目的 观察bcl-2基因在缺氧缺血性脑损伤(HIBD)后细胞凋亡中的表达，探讨新生大鼠HmD后神经细胞凋亡的分子机制。方法 54只7日龄新生SD大鼠随机分为1个对照组和8个实验组。给动物吸入含有92％氮气和8％氧气混合气体建立新生大鼠HIBD动物模型，分另q在脑损伤后不同时间点(0．5、1、3、6、12、24、48、72h等)断头处死动物，取海马组织，用免疫组织化学方法检测海马脑神经细胞凋亡及bcl-2基因表达情况。结果 HIBD1h内未见凋亡细胞出现，3h开始出现，并在48h达高峰，之后逐渐下降。bcl-2蛋白阳性细胞在HIBD后立即出现，6h达到高峰，之后渐下降。结论 HIBD后bd-2基因表达在脑神经细胞凋亡过程中起一定作用。在一定时间范围内,bcl-2基因表达与脑神经细胞凋亡呈负相美。

Relationship between expression of bcl-2 gene and neuronal apoptosis in neonatal rats with hypoxic-ischemic brain damage

Objective To observe the expression of bcl-2 gene in cell apoptosis of neonatal rats followed by hypoxic-ischemic brain damage(HIBD) and investigate the mechanism of neuronal apoptosis after HIBD.Methods Fifty-four neonatal SD rats were used in 1 sham-operated group and 8 trial groups. The models of HIBD were established in neonatal rats by inhaling the mixed gases of 92 % N 2 and 8 % O 2, the animals were sacrificed by dislocation their heads at different time points(0.5,1,3,6,12,24,48,72 h), the hippocampus were dissected for morphological analysis. The neuronal apoptosis and the expression of bcl-2 gene in hippocampus were detected by the methods of immunohistochemistry. Results The apoptotic cells appeared at the time point of 3 h, and reached the peak at 48 h, then decreased. The positive cell of bcl-2 protein increased from the time point of 30 min and reached the peak at 6 h and then decreased gradually following HIBD. Conclusion The expression of bcl-2 gene plays a role in the process of neuronal apoptosis following HIBD.