新生大鼠缺氧缺血脑损伤后bcl-x mRNA的表达

Expression of bcl x mRNA in the neonatal rats following cerebral hypoxia ischemia

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。

Objective To study the changes on the expression of bcl x mRNA follo wing hypoxia ischemia(HI) in the neonatal rat brain and the relationship between bcl x mRNA expression and apoptosis in the hypoxic ischemic developing brain. Methods The animal models of HI brain damage were made. Rapid competitive reverse transcriptase PCR(RT PCR) was used to analyze the expression of bcl x mRNA semi quantity in the hemisphere subjected to both ligation and hypoxia at different time points after HI. The effect of different hypoxic time of 1.5 h,2.5 h and 3.5 h on the expression of bcl x mRNA was also evaluated based on the same ischemic models. Results The expression of bcl xs (short form) mRNA in the neonatal rat brain increased markedly at the termination of hypoxic exposure, peaked at 24 h, and then decreased gradually and returned to baseline at 7 d. The levels of bcl xs mRNA increased with prolonging the duration of hypoxia. The significant differences were found between 1.5 h, 2.5 h and 3.5 h hypoxia group, respectively. The peak time of the overexpression of bcl xs mRNA was coordinate with the peak of apoptosis following HI. HI had no effect on the expression of bcl xl(long form) mRNA.Conclusion HI could increase the expression of bcl xs mRNA in the neonatal rat brain. Within a certain extent, the expression of bcl xs was positively related to the degree of hypoxia. The overexpression of bcl xs could play a role in the induction of apoptosis following cerebral HI.