实验性蛛网膜下腔出血后海马CA1区神经元凋亡的研究

目的探讨实验性蛛网膜下腔出血（SAH）后海马CA1区神经元凋亡及CD95（Fas）分子启动的死亡信号转导机制.方法枕大池二次注血法制备蛛网膜下腔出血模型,HE染色和激光扫描共焦显微镜观察海马CA1区神经元细胞形态学改变,应用逆转录聚合酶链反应（RT-PCR）检测SAH后海马CA1区CD95（Fas）分子启动的死亡信号转导通路蛋白Fas、FasLmRNA的表达变化.结果蛛网膜下腔出血后6 h海马CA1区神经元凋亡细胞开始出现,3～7 d呈典型凋亡细胞形态学改变.Fas、FasLmRNA的表达在蛛网膜下腔出血后呈上升趋势,3 d时达最高,7 d时仍显著高于正常组,14 d时趋于正常. 结论 CD95（Fas）分子启动的死亡信号转导通路在SAH后海马CA1区神经元凋亡中可能起重要作用.

STUDY ON THE NEURONAL APOPTOSIS IN THE HIPPOCAMPAL CA1 REGION AFTER EXPERIMENTAL SUBARACHNOID HEMORRHAGE

Objective To investigate the mechanism of neuronal apoptosis in hippocampal CA1 region and the death signaling transduction pathway initiated by CD95(Fas) molecules during cerebral vasospasm(CVS) after subarachnoid hemorrhage(SAH). Methods SAH model was developed by injecting arterial blood twice the citernamagna.The morphological changes of the neurons were studied by light microscope and laser scanning confocal microscope.RT-PCR was performed for detecting the expression changes of Fas,FasLmRNA. Results Neurons in the hippocampal CA1 region after SAH showed typical apoptotic features under light microscope and confocal microscope.The expressions of Fas,FasLmRNA in hippocampus increased in SAH group,reached the highest level 3 days after SAH and still were significantly higher 7 days after SAH compared with normal group and then decreased to normal 14 days after SAH.Conclusion The death signaling transduction pathway initiated by CD95 molecules may play important roles in hippocampus neuronal apoptosis following SAH.