大鼠蛛网膜下腔出血迟发性血管痉挛神经细胞凋亡及其相关基因表达变化研究

Apoptosis and expression of its related genes in cerebral vasospasm(CVS) model after subarachnoid hemorrhage in rats

目的 从细胞凋亡的角度阐明 SAH后 CVS及其迟发性神经功能缺损的发生机制。方法 TU NEL、RT- PCR检测细胞凋亡及其相关调控基因 ICE及 Bcl- XL在脑神经组织中 m RNA表达变化。结果 TU NEL检测发现对照组大脑皮层偶见散在凋亡神经细胞 ,SAH后 30 m in海马、皮层、及基底节区均可见凋亡细胞开始出现 ,SAH后 3d,凋亡细胞开始增多 ,血管内皮细胞、血管平滑肌细胞亦可见凋亡细胞开始出现 ,SAH后 7d凋亡细胞明显增多达高峰 ;SAH后 30 m in、3d、7d ICE m RNA在脑神经组织中表达均高于对照组 ,Bcl- XL m RNA表达均低于对照组。结论 SAH后 CVS可诱导脑神经组织发生细胞凋亡 ,这种凋亡改变与凋亡调控基因 ICE及 Bcl-X L在脑神经组织中的表达变化有关。

Objective In order to confirm the mechanism of the apoptosis of brain cells,and to explain the pathogenesis of delayed nerve injury and CVS after SAH. Methods To detect the apoptosis of nerve cells and to determine the expression of ICE and Bcl-XL mRNA related to apoptosis in brain tissues,TUNEL and RT-PCR were applied. Results Scattered apoptosis nerve cells could be seen at the zone of hippocampus,cortical area and basal ganglion in CVS rat 30 minites after SAH in control group by TUNEL. The apoptosis cells increased at the zone and the cells could be found in endothelial cells of vessels and smooth muscle cells of vessels 3 days after SAH,the number of apoptosis cells reach the most 7 days after SAH. The expression of ICE mRNA after SAH was markedly higher than the control group,and the expression of Bcl-XL mRNA after SAH was markedly lower than the control. Conclusion CVS after SAH can induce the apoptosis of nerve cells in brain tissues. This may relate to the change of expression of ICE or Bcl-XL.