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探讨新生动物缺氧缺血性脑损伤后细胞死亡相关基因bcl x ,bax表达的变化规律及其与神经细胞凋亡的关系。建立新生大鼠缺氧缺血性脑病动物模型 ,应用快速竞争性RT PCR及原位末端标记法观察脑缺氧缺血后不同时间点缺氧缺血侧大脑组织中bcl x ,baxmRNA的表达及神经细胞凋亡的情况。结果显示缺氧缺血后新生大鼠脑bcl xsmRNA的表达自缺氧结束后即刻即有明显增强 ,2 4h达高峰 ,此后逐渐下降 ,7d时回复至正常基线水平。而baxmRNA的表达自缺氧缺血后 2h开始明显增加 ,2 4h达高峰 ,7d时回复至正常基线水平。缺氧缺血侧脑组织中凋亡细胞数亦自缺氧缺血后 6h明显增多 ,并于 2 4h达高峰。bcl xs ,baxmRNA的表达高峰与缺氧缺血后脑细胞凋亡的高峰时相相吻合。缺氧缺血对bcl xlmRNA的表达无影响。研究表明缺氧缺血可使新生大鼠脑bcl xs ,baxmRNA的表达增强和凋亡细胞增加 ,但对bcl xlmRNA的表达无影响。bcl xl bax的比值在缺氧缺血后脑细胞凋亡的调控过程中起重要作用
To investigate the changes of cell death-related genes bcl x, bax expression and the relationship with the apoptosis of neurons after neonatal hypoxic-ischemic brain damage. To establish an animal model of hypoxic-ischemic encephalopathy in neonatal rats, the expression of bcl x, bax mRNA in hypoxic-ischemic brain tissue at different time points after hypoxia-ischemia was detected by rapid competitive RT-PCR and in situ end-labeling Neuronal apoptosis. The results showed that the expression of bcl xsmRNA in hypoxic-ischemic brain tissue increased immediately after hypoxia, peaked at 24 hours, then decreased gradually and returned to normal baseline level at 7th day. However, the expression of bax mRNA increased significantly from 2h after hypoxic-ischemic insult, reaching the peak at 24h and returned to normal baseline at 7d. The number of apoptotic cells in hypoxic ischemic brain tissue also increased significantly from 6h after hypoxic-ischemia, and peaked at 24h. The peak of bcl xs and bax mRNA expression coincided with the peak phase of apoptosis after cerebral ischemia and hypoxia. Hypoxia-ischemia had no effect on the expression of bcl xlmRNA. Studies have shown that hypoxia-ischemia can make newborn rat brain bcl xs, bax mRNA expression increased and apoptotic cells increased, but no effect on bcl xlmRNA expression. The ratio of bcl xl bax plays an important role in the regulation of apoptosis in brain cells following hypoxia-ischemia