脑缺血大鼠脑组织胰岛素受体基因表达特点及其机制

目的 观察局灶性脑缺血再灌注大鼠脑组织胰岛索受体基因表达的分布及不同再灌注时间的表达特点，探讨胰岛素受体参与脑缺血再灌注后组织病理生理变化的可能机制。方法 采用改良gealong线栓法建立大鼠大脑中动脉梗死模型。免疫组化法检测大鼠梗死组和正常对照组不同再灌注时间脑组织胰岛素受体蛋白表达。原位杂交法检测脑组织胰岛素受体mRNA表达。结果 梗死组脑组织胰岛素受体mRNA及蛋白表达较对照组明显增加（P〈0．01），再灌注12h达高峰，胰岛素受体阳性表达主要分布于梗死灶周围半暗带区神经元细胞浆、细胞膜、部分神经胶质细胞、血管内皮细胞等处；随再灌注时间延长，上述细胞变化各异。结论 脑缺血再灌注大鼠脑组织胰岛素受体基因和蛋白水平表达增加，半暗带区神经元、部分神经胶质细胞及血管内皮细胞等阳染细胞可能参与脑缺血后组织细胞的能量代谢、促新生细胞形成等病理生理调节过程，胰岛索受体在缺血区血管内皮细胞高表达提示其可能在缺血区血管的病理生理变化中起某种调节作用；胰岛素受体在不同细胞中表达增高可能是缺血脑组织对抗缺血缺氧损伤的自身保护机制之一。

Distribution and characters of insulin receptor gene in the brain tissue in rats with cerebral ischemia

Objective: To observe the distribution and the characters of insulin receptor gene in the brain tissue during different reperfusion time after focal cerebral ischemia reperfusion in rats,to investigate the possible machanisms of insulin receptor participating in the pathophysiological changes after cerebral ischemia reperfusion.Methods: The models of the middle cerebral artery occlusion were made by improved zealong's method.The expressions of insulin receptor protein in the brain tissues were investigated by immunohistochemistry staining.The expressions of insulin receptor mRNA were investigated by in situ hybridization staining.Results: There was a significant increase of insulin receptor mRNA and protein in the infarction tissues compared with control groups(P<0.01),peaked at 12h;The insulin receptor distributed mainly in the cytoplasm and cytomembrane of neurons in the ischemic penumbra zones,some neuroglia cells,vascular endothelium cells,et al;Along with the reperfusion time,the expressions of the cells talked above changed differently.Conclusions: There was an obvious increase of insulin receptor gene and protein in the cerebral ischemia reperfusion tissues in rats.The positive cells such as neuron,neuroglia cells,vascular endothelium cells possibly participated in regulating the processes of energy metabolism of cells and neovascularization.It implied that the high expressions of insulin receptors in vascular endothelium cells in ischemic zones possibly participated in regulating the pathophysiological changes of the blood vessels in ischemic zones;The higher expressions of insulin receptors in different cells were possibly one of the self-protective machanisms in which the ischemic tissues confront the anoxemia injury.