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