摘要
目的探讨大鼠脑缺血再灌注后神经细胞凋亡及Fas凋亡通路相关因子Fas相关死亡域蛋白(fas-associated death domain,FADD)、半胱天冬酶-8(Caspase-8)及Flice(即Caspase-8)抑制蛋白(FLICEProfilin,FLIP)的mRNA及蛋白表达。方法线栓法制备大脑中动脉梗死模型(MCAO),TUNEL法检测神经细胞凋亡,RT-PCR法及免疫组化法检测不同实验组中FADD、Caspase-8及FLIP的mRNA及蛋白表达。结果大鼠脑缺血再灌注后各时间点神经细胞凋亡,FADD、Caspase-8及FLIP的mRNA和蛋白表达均明显增强(P<0.05～0.001)。结论大鼠脑缺血再灌注后神经细胞凋亡数增加,Fas-FADD-Caspase-8凋亡通路可能为其重要凋亡通路之一,抗凋亡因子FLIP mRNA和蛋白表达短暂升高,可能有拮抗脑缺血再灌注后神经细胞凋亡的作用。
[Objective] To study the neuronal apoptosis and the expression of the mRNA and protein of Fas-associated death domain protein （FADD）, Caspase-8 and Flice Profilin （FLIP） in rat after ischemia-reperfusion. [Methods] 60 SD rats were divided into 4 groups randomly： normal group （n =10）, sham-operated group （n =10）, cerebral ischemia-reperfusion model group （n =40）. The neuronal apoptosis was detected by the method of TUNEL, the expression of the mRNA and protein of FADD, Caspase-8 and FLIP were respectively evaluated by methods of RT-PCR and immunohistochemistry. [Results] Compared with normal group and sham-operated group the number of apoptotic cell and the expression level of the mRNA and protein of FADD, Caspase-8 and FLIP in the rat of model group increased significantly （P 〈0.05-0.001）. [Conclusions] The neuronal apoptosis increased significantly in rats after ischemia-reperfusion, the Fas-FADD-Caspase-8 apoptotic signal transduction pathways may be one of the important apoptotic signal transduction pathways in them, the transient upregulation of FLIP may inhibit neuronal apoptosis following cerebral ischemia-reperfusion.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2009年第1期64-67,71,共5页
China Journal of Modern Medicine
