【摘要】 目的探讨全脑缺血-再灌注对成年大鼠海马CA1区GAD65表达的影响及意义。方法成年雄性SD大鼠24只,随机分为3组:假手术组(SH)、缺血-再灌注3d组(IR-3)及缺血-再灌注7d组(IR-7),每组8只。采用四动脉阻断法制作全脑缺血-再灌注模型,应用免疫组织化学方法检测海马CA1区谷氨酸脱羧酶(glutamic acid decarboxylase,GAD)同工酶GAD65的表达变化。结果与假手术组相比,IR-3组GAD65的表达明显增多,IR-7组恢复正常。结论GABA能中间神经元对缺血相对耐受;全脑缺血-再灌注3dGAD65的表达增多可能是一种代偿性的机制,以减轻脑缺血后的高兴奋性。更多还原

【Abstract】 Objective To observe the effect of global ischemia-reperfusion on the expression of GAD65 in the hippocampal CAl region of adult rats.Methods 24 male SD rats were randomly divided into three groups:sham-operation group(SH,n=8),ischemia-reperfusion three days(IR-3,n=8) and seven days group(IR-7,n=8).Global ischemic episode was achieved by 4-vessel occlusion.Immunohistochemical method was applied to observe the expression of GAD65 in hippocampal CAl region.Results At ischemia-reperfusion third day,the immunoreactivities of the GAD 65 were markedly elevated in the CA1 region compared with sham operated group,but the immunoreactivities recovered to the sham level at ischemia-reperfusion seventh day.Conclusion GABAergic interneurons relatively resistant to ischemia-reperfusion injury,and the increasing expression of GAD65 3d after ischemia-reperfusion can be a compensatory mechanism to reduce the hyperexcitability associated with ischemia-reperfusion.更多还原