摘要
目的 探讨脑创伤后bcl-xL 和bax在mRNA水平的变化规律。 方法 应用RT -PCR法分别检测大鼠液压脑损伤后不同时程bcl-xL 和baxmRNA表达情况 ;采用凋亡原位末端标记、电镜超微结构、DNA凝胶电脉 ,观察脑创伤后细胞凋亡的形态和生化特征。 结果 在打击组所有标本中均可测得bcl-xL mRNA和baxmRNA的表达。bcl-xL mRNA的改变出现在伤后 6h ,早于细胞凋亡的发生 ,此时致伤侧半球bcl -xL mRNA扩增产物明显少于对侧 ,为对侧的 (6 7.42±7.5 4) % (P <0 .0 1) ;伤后 3d到达低谷 ,为对侧的 (39.97± 3.6 1) % ,以后逐渐恢复。伤后 6h、1dbaxmRNA无显著变化 ,致伤侧半球baxmRNA在伤后 3d升高为对侧半球的 (2 0 3.95± 17.5 3) %(P <0 .0 1) ,伤后 3～ 7d逐渐下降。 结论 细胞凋亡及其调节基因的表达间具有一致性 :脑创伤后早期 ,bcl-xL mRNA下调危及细胞生存 ;
Objective To investigate the alterations of bcl-2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods Male Sprague-Dawley rats were subjected to lateral fluid perfusion brain injury(FPI) of moderate severity. bcl-x L and bax mRNA expression was detected by RT-PCR. In addition to morphological evidence of apoptosis, TUNEL histochemistry was used to identify DNA fragmentation in situ at both light and electron microscopic levels, the characteristic internucleosomal DNA fragmentation of apoptosis was demonstrated by DNA gel electrophoresis. Results The apoptotic response to trauma was regionally distinct and might be involved in both acute and delayed patterns of cell death. bcl-x L mRNA decreased in the ipsilateral hemisphere to the impact site 6 h after injury (67.42%±7.54%, P <0.01). The decrease in bcl-x L mRNA preceded apoptosis, which was observed 24h after injury. This was the main cause of down-regulation of the ratio of bcl-x to bax in the acute period (minutes to hours) following lateral fluid perfusion brain injury. bax mRNA was observed to rise slowly , doubling at 3rd day after injury, then returned to the sham level slowly. The delayed cell death (days to weeks) involved the up-regulation of pro-apoptotic gene bax. Conclusions The decreased expression of bcl-x L mRNA and increased expression of bax mRNA coincide with apoptosis following brain injury. The bcl-2 gene family is involved in neuronal apoptosis after TBI, and the mRNA expression alterations of the family members lead the neuronal cells to apoptosis.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2001年第4期209-211,共3页
Chinese Journal of Trauma
基金
军队"九五"指令性课题(颅脑战创伤脑保护的基础与应用研究)资助项目!(96L0 36)
