【摘要】 目的探讨低氧预适应(HPC)对脑中动脉梗塞(MCAO)小鼠脑的保护作用,以及缺血皮层内经典型蛋白激酶C(cPKC)βⅡ和γ膜转位水平的改变。方法健康雄性BALB/c小鼠(18~22 g,8~10周)随机分为:H0假手术(n=6),H0缺血(n=6),H4假手术(n=6)和H4缺血(n=6)组。运用整体低氧预适应模型和脑中动脉梗塞缺血模型,结合2,3,5氯-化三苯基四氮唑(TTC)染色、SDS聚-丙烯酰胺凝胶电泳(SDS-PAGE)和蛋白印迹(W estern blot)等分子生物学技术,观察脑梗死面积、缺血区密度值和水肿率,以及MCAO小鼠缺血皮层组织内PKCβⅡ和γ膜转位水平的变化。结果研究发现,HPC可明显减小MCAO导致的鼠脑梗死面积(P<0.05),降低缺血区吸光度值(P<0.05)和水肿率(P<0.05);与H0假手术组相比,缺血组小鼠皮层半影区cPKCβⅡ和γ膜转位水平显著降低(P<0.05);与H0缺血组小鼠皮层半影区相比,H4缺血组小鼠皮层半影区内PKCβⅡ和γ膜转位水平明显增高(P<0.05)。结论HPC可能通过增加MCAO小鼠皮层组织内cPKCβⅡ和γ的膜转位水平,对缺血损伤起保护作用。更多还原

【Abstract】 Objective To explore the protection of hypoxic preconditioning(HPC) on middle cerebral artery occlusion(MCAO)-induced brain injuries of mice and the changes in protein kinase C(PKC) βⅡ and γ membrane translocation in ischemic cortex of MCAO mice.Methods Male BALB/c mice(18～22 g,8～10 w) were randomly divided to H0+Sham(n=6),H0+Ischemia(n=6),H4+Sham(n=6) and H4+Ischemia(n=6) group.Using our unique hypoxic preconditioned mouse model and middle cerebral artery occlusion mouse model,combined with TTC staining,SDS-PAGE and Western blot,we observed the changes in infarction sizes,density,edema ratio,and changes in cPKCβⅡ and γ membrane translocation in ischemic cortex of MCAO mice.ResultsHPC significantly reduced infarction size(P<0.05),density of infarct area(P<0.05) and edema ratio(P<0.05).As compared with H0+sham group,cPKCβⅡ and γ membrane translocation levels in penumbra of ischemic cortex decreased significantly(P<0.05).Whereas cPKCβⅡ and γ membrane translocation levels in penumbra of ischemic cortex in H4+Ischemia group increased significantly compared with that of mice in H0+Ischemia group(P<0.05).Conclusion Hypoxic preconditioning increased levels of cPKCβⅡ and γ membrane translocation in penumbra of middle cerebral artery occluded mice,which may be involved in the protective effect of HPC to severe ischemic injury.更多还原