Abstract:Objective：To investigate the mechanism of alternation of PKC activify in liver ischemia preconditioning(IP).
Methods ：After establishment of rat liver IP model, PKC inhibitor and activator were utilized to analyze the phosphorylation of PKC and P44/42MAPKs and HSP expression, and cellular structure was also observed. All of the data were statistically analyzed.
Results：Compared with the control group without IP, the phosphorylation of PKC was significantly increased in IP treated models and PKC activated group(P< 0.01), and P44/42 MAPKs and expression of HSP 70 were also obviously increased, but with little change of hepatic cellular structure. In contrast, opposite changes were found in PKC inhibited groups, the phosphorylation PKC was decreased in PKC inhibited group(P< 0.01) and marked changes in hepatic cellular structure.
Conclusions：The IP model has shown that PKC activation plays a pivotal role in the activation of P44/42 MAPKs pathway that participates in the preservation of liver cells. At the same time, HSP expression is regulated by signals in P44/42 MAPKs pathway.