TLR4及MyD88在大鼠局灶性脑缺血耐受过程中的作用

目的本实验拟探究经脑缺血预处理后Toll样受体4（TLR4）及其下游髓样分化因子88（MyD88）蛋白在脑缺血耐受中的作用。方法采用改进的大鼠大脑中动脉线栓法构造大鼠脑缺血预处理模型，取大鼠脑组织后应用2，3，5-氯化三苯基四氮唑（Trc）染色观察鼠脑梗死面积变化，干湿法探究脑水肿程度改变，并通过Westernblot横向对比各组TLR4及MyD88蛋白表达情况。结果缺血处理后大鼠当其再次面临缺血再灌注损伤时，TLR4蛋白和MyD88蛋白表达在各观察时间点均呈现了不同程度的降低，且梗死面积及脑水肿程度也有所降低。结论经脑缺血预处理后脑组织可产生对致死性再灌注损伤的耐受，这种耐受是通过TLR4及MyD88蛋白的下调表达实现的并具有一定的时效性。

The role of TLR4 and MyD88 proteins in rat focal cerebral ischemic tolerance with ischemic precondition

Objective To explore the functions of Toll-like receptor 4 （TLR4） and myeloid differentiation factor 88 （MyD88） proteins in cerebral ischemie tolerance induced by ischemic precondition. Methods The improved middle cerebral artery occlusion method was used to construct preconditioning ischemie rat brain model. The infarction area was detected by 2, 3, 5-triphenyltetrazolium （TIE） stain of brain tissues and the water content of brain tissues was detected using the dry-wet weight technique. The TLR4 with MyD88 proteins expression was compared by Western blot. Results Expressions of TLR4 and MyD88 showed a different degree of reduction in precondition ischemic rat brain at different time points after ischemia and reperfusion injury and the infarct area and brain tissue water content were also decreased. Conclusion Down-regulated expression of TLR4 and MyD88 proteins is closely related to the generation of ischemic tolerance after isehemic precondition with a characteristic of time effectiveness.