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目的:探讨虎纹蜘蛛毒素-I(HWTX-I)与由Fas分子启动的死亡信号转导通路之间的关系及可能的神经保护作用分子机制。方法:48只SD大鼠随机分为假手术组、生理盐水组及用药组三组,每组16只,采用改良的Pulsinelli“四血管阻断法”并结合蛛网膜下腔置管术构建全脑缺血再灌注损伤大鼠模型。免疫组织化学法检测海马组织CA1区Fas、FasL、FADD蛋白水平表达,RT-PCR法检测海马组织死亡信号转导通路相关因子Fas、FasL、FADD核酸水平表达。结果:免疫组化法检测结果显示,生理盐水组、用药组Fas、FasL和FADD蛋白表达高于假手术组,差异均有统计学意义(P<0.05,P<0.01),用药组Fas、FasL和FADD蛋白表达低于生理盐水组,差异均有统计学意义(P<0.05,P<0.01);RT-PCR检测结果显示,假手术组Fas、FasL、FADDmRNA表达低于生理盐水组和用药组,差异均有统计学意义(P<0.05,P<0.01),用药组Fas、FasL、FADDmRNA表达均低于生理盐水组,差异均有统计学意义(P<0.05,P<0.01)。结论:HWTX-I蛛网膜下腔用药对全脑缺血再灌注损伤大鼠海马组织具有一定的神经保护作用,其机制可能是通过抑制Fas分子启动的死亡信号转导通路激活而发挥作用。
Objective: To explore the molecular mechanism of the relationship between HWTX-I and the death signal transduction pathway initiated by Fas molecules and the possible neuroprotective effect. Methods: Forty eight Sprague-Dawley rats were randomly divided into three groups: sham-operation group, saline group and medication group. Each group had 16 rats in each group. The modified Pulsinelli “four-vessel occlusion” method combined with subarachnoid catheterization To establish a rat model of global cerebral ischemia-reperfusion injury. The expression of Fas, FasL and FADD protein in hippocampal CA1 region was detected by immunohistochemistry. The expressions of Fas, FasL and FADD in hippocampus were detected by RT-PCR. Results: The results of immunohistochemistry showed that the expressions of Fas, FasL and FADD protein in normal saline group and treatment group were significantly higher than those in sham operation group (P <0.05, P <0.01) (P <0.05, P <0.01). The results of RT-PCR showed that the expressions of Fas, FasL and FADD mRNA in the sham group were lower than those in the saline group and the drug group (P <0.05, P <0.01). The expressions of Fas, FasL and FADD mRNA in the treatment group were significantly lower than those in the normal saline group (P <0.05, P <0.01). Conclusion: The subarachnoid administration of HWTX-I can protect neurons in hippocampus of rats with global cerebral ischemia-reperfusion injury possibly by inhibiting the activation of death signal transduction pathway initiated by Fas molecule.