大鼠脑创伤后Fas mRNA表达与细胞凋亡关系及GM-1的脑保护作用

目的 通过观察大鼠脑创伤后海马区Fas mRNA的表达及细胞凋亡的情况，进一步探讨脑创伤后细胞凋亡的机制和GM-1的脑保护作用。方法 建立Marmarou颅脑创伤模型，同时给予GM-1治疗，采用TUNEL和原位杂交方法观察细胞凋亡及Fas mRNA在脑创伤后的变化规律。结果 脑创伤后海马区神经细胞过度地表达Fas mRNA，并且该区出现明显的神经细胞凋亡，GM-1能够使Fas mRNA的表达高峰及神经细胞凋亡高峰下调。结论 Fas的过度表达可能是脑创伤后神经细胞凋亡的重要原因。GM-1可能通过抑制Fas的表达，减少神经细胞凋亡发挥脑保护作用。

The Relationship Between Expression of Fas mRNA and Apoptosis after Traumatic Brain Injury in Rats and the Role of GM-1 in Protecting the Brain

Objective To explore the mechanism of apoptosis after traumatic brain injury (TBI) in rats and elucidate the role of GM-1 by detecting the expression of Fas mRNA and apoptosis in hippocampi. Methods After creating the model of Marmarou cranio-cerebral trauma and offering GM-1 therapy, we observed the expression of Fas mRNA and apoptotic cell death using in situ hybridization and terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling(TUNEL) technique. Results Increased expression of Fas mRNA and increased apoptotic cells in hippocampi after TBI were observed. GM-1 could decrease the expression of Fas mRNA and apoptotic cell death. Conclusion The increased expression of Fas mRNA may be a noteworthy cause of apoptotic cell death after traumatic brain injury. GM-1 may play a protective role by way of decreasing the expression of Fas mRNA and apoptotic cell death.