【摘要】 目的:观察PTD-kallikrein对大鼠MCAO模型缺血再灌注损伤的保护作用,并探讨其可能的作用机制。方法:以化学交联法构建PTD-kallikrein,鉴定PTD-kallikrein对血脑屏障的通透性,并测定PTD肽段对原代神经元、星形胶质细胞及PC12细胞的毒性作用,制备大鼠MCAO模型,梗死90min后再灌注,并分为生理盐水组、Kallikrein组、PTD-kallikrein组和PTD-kallikrein+B2抑制剂组。再灌注后24h,分别用NSS量表测定神经功能,TTC染色测定梗死灶体积,ELISA测定梗死灶细胞因子IL-1β、TNF-α及PGE2的含量。结果:PTD-kallikrein能通过血脑屏障,1μmol/LPTD肽段对上述3种细胞无毒性,10μmol/LPTD肽段对原代神经元和PC12细胞有轻度毒性;PTD-kallikrein能显著改善脑缺血导致的神经功能障碍、减小梗死体积、抑制细胞因子IL-1β、TNF-α及PGE2的释放,B2受体抑制剂能明显抑制PTD-kallikrein的神经保护作用。结论:PTD-kallikrein对大鼠MCAO模型缺血再灌注损伤有显著保护作用,并且很可能通过B2受体介导而发挥该功效。更多还原

【Abstract】 Objective:The protective effect of PTD-kallikrein on cerebral ischemia-reperfusion injury induced by MCA occlusion has been explored in rats.Methods:PTD-kallikrein was prepared by chemical synthesis.Cerebral ischemia-reperfusion model was generated by occluding the left middle cerebral artery(MCA)for 90 minutes through the intraluminal thread technique and followed by reperfusion in rats.The rats were then treated by normal saline,Kallikrein,PTD-kallikrein and PTD-kallikrein plus bradykinin B2 receptor antagonist individually.After the neurologic functions were appraised by NSS,the rats were decapitated.The infarct volume was determined by TTC stain and the concentrations of cell factors IL-1β,TNF-α,and PGE2 in ischemic tissues were measured by ELISA.Results:PTD-kallikrein was found to improve the disordered neurologic functions caused by cerebral ischemia,to decrease the infarct volume,and to inhibit the releases of IL-1β,TNF-α,and PGE2.However,Bradykinin B2 receptor antagonist was discovered to significantly block the effect of PTD-kallikrein.Conclusion:PTD-kallikrein has a neuroprotective action in the cerebral ischemia-reperfusion injury induced by MCA occlusion in rats to some degree,possibly through bradykinin B2 receptor system.更多还原