论文部分内容阅读
目的 探讨新生大鼠脑缺氧缺血后死亡相关基因 bcl- x m RNA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缺血侧大脑组织中 bcl- x m RNA的表达进行半定量分析 ,并在相同缺血基础上观察缺氧 1.5小时、2 .5小时和 3.5小时对 bcl- x m RNA表达的影响。结果 缺氧缺血后 ,新生大鼠脑 bcl- xs(bcl-x短型 ) m RNA的表达自缺氧结束后即刻即有明显增强 ,2 4小时达高峰 ,此后逐渐下降 ,7天时回复至正常基线水平。随着缺氧时间的延长即缺氧程度的加重 ,bcl- xs m RNA的表达有增强趋势 ,缺氧 1.5小时组、2 .5小时组及 3.5小时组之间 bcl- xs m RNA表达水平的差异均具显著性意义 (P<0 .0 1)。bcl- xs m RNA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- xl(bcl- x长型 ) m RNA的表达无影响。结论缺氧缺血可诱导新生大鼠脑 bcl- xs m RNA表达增强。在一定范围内 ,其表达强度与缺氧程度成正相关。 bcl-xs过表达在缺氧缺血后脑细胞凋亡的调控过程中起着一定的作用
Objective To investigate the changes of the expression of bcl-x m RNA in neonatal rats with hypoxic-ischemic brain damage and its relationship with apoptosis induced by hypoxic-ischemic brain damage. Methods The animal models of neonatal hypoxic-ischemic encephalopathy were established. The expression of bcl-xm RNA in ischemic brain tissue was detected by rapid competitive RT-PCR at different time points after hypoxia-ischemia. The effects of hypoxia for 1.5 hours, 2.5 hours and 3.5 hours on the expression of bcl-xm RNA were observed on the same ischemia. Results After hypoxia-ischemia, the expression of bcl-xs (bcl-x short) m RNA in neonatal rats increased significantly immediately after hypoxia, reaching a peak at 24 hours and then decreased gradually. After 7 days, Normal baseline level. The expression of bcl-xs m RNA tended to increase with the increase of hypoxia time, the expression of bcl-xs m RNA in hypoxia 1.5 hours, 2.5 hours and 3.5 hours The difference was significant (P <0.01). The peak expression of bcl-xs m RNA coincided with the peak phase of apoptosis after cerebral ischemia and hypoxia. Hypoxia-ischemia had no effect on the expression of bcl-xl (bcl-x long) m RNA. Conclusion Hypoxia and ischemia can induce the expression of bcl-xs m RNA in neonatal rat brain. Within a certain range, its expression intensity and the degree of hypoxia is positively correlated. Overexpression of bcl-xs plays a role in the regulation of apoptosis after cerebral ischemia and hypoxia