基础医学与临床 ›› 2009, Vol. 29 ›› Issue (2): 129-134.

• 研究论文 • 上一篇    下一篇

蛋白激酶C II和 参与低氧预适应降低脑中动脉阻塞所致鼠脑缺血性损伤

杨巍巍 江君 卜祥宁 张楠 谢培伦 张伯民 李俊发   

  1. 首都医科大学神经生物系 首都医科大学神经生物系 首都医科大学神经生物学系疼痛生物医学研究所 首都医科大学疼痛生物医学研究所 首都医科大学神经生物系
  • 收稿日期:2008-08-06 修回日期:2008-12-02 出版日期:2009-02-25 发布日期:2009-02-25
  • 通讯作者: 李俊发

cPKC II and participated in the attenuation of MCAO-induced brain injuries of mice following hypoxic preconditioning

Wei-wei YANG, Jun JIANG, Xiang-ning BU, Nan ZHANG, Pei-lun XIE, Bo-min ZHANG, Jun-fa LI   

  1. Department of Neurobiology and Beijing Institute for Neuroscience, Capital Medical University Department of Neurobiology and Beijing Institute for Neuroscience, Capital Medical University Institute for Biomedical Sciences of Pain, Department of Neurobiology, Department of Neurobiology and Beijing Institute for Neuroscience, Capital Medical University
  • Received:2008-08-06 Revised:2008-12-02 Online:2009-02-25 Published:2009-02-25
  • Contact: Jun-fa LI

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) II和 膜转位水平的改变。方法 健康雄性BALB/c小鼠(18~22g,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(Western 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PKC II和 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cPKC II和 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PKC II和 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cPKC II和 的膜转位水平,对缺血损伤起保护作用。

关键词: 脑中动脉梗塞, 低氧预适应, 蛋白激酶C, 膜转位

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) II and membrane translocation in ischemic cortex of MCAO mice. Methods Male BALB/c mice (18-22g, 8-10w) 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 cPKC II and 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, cPKC II and membrane translocation levels in penumbra of ischemic cortex decreased significantly (p<0.05). Whereas cPKC II and 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 cPKC II and membrane translocation in penumbra of middle cerebral artery occluded mice, which may be involved in the protective effect of HPC to severe ischemic injury.

Key words: Middle cerebral artery occlusion (MCAO), hypoxic preconditioning, protein kinase C, membrane translocation

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