P>ObjectiveTo investigate the changes in p-Akt and Bid after ischemia reperfusion(I/R)injury and ischemic postconditioning(IP),and the relationship between p-Akt and IP. MethodsFocal ischemia was generated by transient middle cerebral artery occlusion(MCAO). Totally 315 male Kunming mice were randomly divided into four groups：Sham group,I/R group,IP group,IP plus LY group.At the right time point,the brain tissue samples were prepaired for brain histology and determination of the experssion of p-Akt and Bid,by means of immunohistochemistry and Western blotting.The volume ratio of the cerebral infarction was estimated by 20 g/L TTC staining. ResultsIn the cytoplasm of nerve cells,the levels of Akt and Bid were higher in I/R mice than those in Sham mice.The expression of p-Akt in the cytoplasm began to increase at the 0.5 hour, increased to the highest level at the 1st hour (EM>P/EM><0.05),and then gradually returned to the basic level.But the expression of Bid began to increase at the 6th hour, increased to the highest level at the 24th hour(EM>P/EM><0.05),and then returned gradually; At the corresponding time,compared with I/R group,the expression of p-Akt increased remarkably in IP group(EM>P/EM><0.05); meanwhile, the expression of Bid decreased significantly in IP group (P<0.05).LY294002,a specific blocker of PI-3K,notably blocked PI-3K/Akt signal pathway and inhibited the protective effects of IP in the brain. The experssion of p-Akt negatively correlated with the activated Bid (EM>r/EM> =-0.826 5, EM>P/EM><0.05).ConclusionThe protective effects of IP in the mice brain is exerted through regulating Akt signal pathway.Perhaps,the up\|regulation of the activation of P1-3K/Akt system is one of the mechanism through which the protective effects of IP can exert .Bid is involved in the process of IP. Akt can regulate the expression of Bid through the death receptor signal pathway./P>