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蛋白激酶CβⅡ和γ参与低氧预适应降低脑中动脉阻塞所致鼠脑缺血性损伤 被引量:5

cPKCβⅡ and γ participated in the attenuation of MCAO-induced brain injuries of mice following hypoxic preconditioning
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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。 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 + Isehemia ( 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. Results HPC 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 cPK CβⅡ and γ membrane translocation levels in penumbra of ischemic cortex in H4 + Isehemia group increased significantly compared with that of mice in H0 + Isehemia 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.
出处 《基础医学与临床》 CSCD 北大核心 2009年第2期129-134,共6页 Basic and Clinical Medicine
基金 国家自然科学基金(30670782 30871219) 国家"973"计划(2006CB5041) 北京市自基金A类项目(5072008) 北京市教育委员会科技计划重点项目(KZ200810025012) 北京市属高等学校人才强教计划项目(京教人[2008]17号) 北京市新世纪百千万人才工程培养经费资助(08-016)
关键词 脑中动脉梗塞 低氧预适应 蛋白激酶C 膜转位 middle cerebral artery occlusion (MCAO) hypoxic preconditioning protein kinase C membrane translocation
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参考文献11

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