目的　探讨新生大鼠脑缺氧缺血后bcl 2mRNA表达的变化及其与脑缺氧缺血所致细胞凋亡的关系。方法　通过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技术对缺氧缺血后不同时间点的实验侧大脑组织中bcl 2mRNA的表达进行半定量分析 ,并在相同缺血基础上观察缺氧 1 5h、2 .5h和 3 5h对bcl 2mRNA表达的影响。结果　缺氧缺血后 ,新生大鼠脑bcl 2mRNA的表达自缺氧结束后 6h开始明显增强 ,1 2h达高峰 ,2 4h回落至较低水平 ,至 72h已基本检测不到。随着缺氧时间的延长即缺氧程度的加重 ,bcl 2mRNA的表达有增强趋势 ,但在缺氧 1 5h组和 2 5h组之间无显著性差异 ,而缺氧 1 5h组或 2 5h组与缺氧 3 5h组之间均具显著性差异 (P <0 0 1 ) ,后者表达更强。结论　缺氧缺血可诱导新生大鼠脑bcl 2mRNA的表达。在一定范围内 ,缺氧越严重 ,其表达越强。但由于严重损伤时蛋白质的合成常受到抑制 ,因此在判断bcl 2mRNA与凋亡的关系时必须结合其产物bcl 2蛋白的合成情况进行分析。 Objective To investigate the changes of bcl-2 mRNA expression in neonatal rats after hypoxic-ischemic brain damage and its relationship with apoptosis induced by hypoxic-ischemic brain damage. Methods The animal model of neonatal hypoxic-ischemic encephalopathy was established. The rapid competitive RT-PCR technique was used to semi-quantitatively analyze the expression of bcl 2 mRNA in the experimental side of the brain at different time points after hypoxia-ischemia. Blood on the basis of hypoxia 15h, 2.5h and 35h on bcl 2 mRNA expression. Results After hypoxia-ischemia, the expression of bcl-2 mRNA in neonatal rat brain increased significantly at 6h after hypoxia, peaked at 12h, dropped to a lower level 24 hours later, and was almost undetectable at 72h. With the extension of hypoxia time, hypoxia, the expression of bcl 2 mRNA tended to increase, but there was no significant difference between hypoxia group 15h and 25h, while hypoxia group 15h or 25h And hypoxia 35h group were significantly different (P <0.01), the latter expression is stronger. Conclusion Hypoxia-ischemia can induce the expression of bcl 2 mRNA in neonatal rats. Within a certain range, the more severe the hypoxia, the stronger its expression. However, due to the severe damage of protein synthesis often inhibited, so in judging the relationship between bcl 2 mRNA and apoptosis must be combined with the synthesis of its product bcl 2 protein analysis.