关键词: 低氧预适应, 脑中动脉阻塞, p38丝裂原激活蛋白激酶, 磷酸化水平

Abstract: Objective To observe the effect of hypoxic preconditioning(HPC) on middle cerebral artery occlusion(MCAO)-induced brain injury of mice and explore the change of p38 mitogen activated protein kinase(p38 MAPK) in neuroprotection of HPC. Methods Male BALB/c mice(18 g-22 g, 8 weeks-10 weeks) were randomly divided into H0 sham, H0, H4 sham and H4 groups. Using our unique hypoxic preconditioned mouse model and middle cerebral artery occlusion mouse model, combined with triphenyltetrazolium chloride(TTC) staining, neurological deficits evaluation, immunohistochemistry and Western blotting, the authors observed the changes of neurological score, brain infarct volume, neuronal injury, p38 MAPK phosphorylation and protein expression levels in the cerebral cortex of mice. Results HPC significantly decreased the neurological score, reduced infarction size, density of infarct area and edema ratio, and attenuated neuronal loss. Compared with the sham control, ischemia increased the phosphorylation levels of p38 MAPK significantly in penumbra of mouse brain. Furthermore, compared with the normoxic control, the phosphorylation levels of p38 MAPK increased more significantly in penumbra of HPC ischemic group. Conclusion p38 MAPK signal pathway might be involved in neuroprotective effect of HPC on focal ischemic brain of mice.

Key words: hypoxic preconditioning, middle cerebral artery occlusion, p38 mitogen activated protein kinase, phosphorylation