Abstract: Objective　To explore the effect of hypoxic preconditioning (HPC) on middle cerebral artery occlusion (MCAO)-induced brain injury of mice and the changes of p38 mitogen activated protein kinase (p38 MAPK) phosphorylation and protein expression levels in the ischemic cortex. Methods　Using our established HPC and MCAO mouse models, healthy male BALB/c mice weighing at 18～20 g were randomly divided into 4 groups: H0 sham, H4 sham, H0 and H4 group. The brain infarct volume and neural injury was determined by 2,3,5-Triphenyltetrazolium chloride (TTC) and Nissl staining. Western blot combined with GelDoc imagine systems were applied to examine the changes in p38 MAPK phosphorylation and protein expression levels in the brain of mice. Results　HPC significantly attenuate the brain injury induced by MCAO (P<0.05). Phosphorylation levels of p38 MAPK in the ischemic core and penumbra increased significantly when compared with H0 sham group (P < 0.05, n = 6 for each group). HPC increased the phosphorylation levels of p38 MAPK in the penumbra and contralateral cortex (P<0.05, n=6). However, there were no significant changes in p38 MAPK protein expression levels. Conclusion p38 MAPK might involved in the attenuation of MCAO-induced brain injury by HPC of mice.

Key words: Cerebral hypoxic preconditioning, Middle cerebral artery occlusion (MCAO), p38 MAPK, phosphorylation, protein expression