Abstract: Objective To explore the effects of hypoxic preconditioning (HPC) on middle cerebral artery occlusion (MCAO)-induced brain injuries and its possible mechanisms. Methods Using our established HPC and MCAO mouse models, and the techniques of 2,3,5-Triphenyltetrazolium chloride (TTC) staining, neurological evaluation, SDS-PAGE and Western blot, we observed the changes in infarction sizes, edema ratio, behavior score, and nPKC membrane translocation in the ischemic core and penumbra of mice following hypoxic exposure and ischemic injuries. Results MCAO could induce three types of cerebral ischemia: cortical, hippocampal and thalamic ischemia (data not shown due to the rare incidence); In the cortical ischemia, HPC significantly reduced infarction size (P<0.05, n=10), density of infarct area (P<0.05, n=10) and edema ratio (P<0.05, n=6); However, HPC only decreased the density of infarct area significantly (P<0.05, n=7) in the hippocampal ischemia; HPC also partially relieved the MCAO-induced neurological deficits of mice; In addition, HPC could prevent the decreased nPKC membrane translocation induced by MCAO in penumbra of mice brain. Conclusion HPC can attenuate MCAO-induced brain injuries, and nPKC may be involved in the neuroprotection.

Key words: HPC, MCAO, TTC staining, penumbra, nPKCepsilon