Ischemic Postconditioning Attenuates Ischemia/Reperfusion-induced Injury Through Activating Inflammatory Signaling Pathways

Abstract

The role of post-treatment in protecting organ ischemia and re-perfusion damage is increasingly recognized, however, its mechanism of the action is not very clear, all in all, it still needs further research. The purpose of this experiment is to investigate whether IPO can reduce I/R-induced liver damage through inhibiting inflammatory signaling pathways in rats. Rats were randomly divided into sham, I/R, IPO and LY294002+IPO groups. The levels of AST and ALT were assessed. The expression levels of IL-1, Akt, NF-κB-P65 and TNF-α were analyzed using western blot analysis. The expression levels of ALT, AST, IL -1, TNF-α and NF-κB-P65 were significant reduction in the IPO group compared with those in the I/R group. Furthermore, the protein expression level of phosphorylated Akt was observed to be significant increase in the livers of the rats in the IPO group compared with those in the I/R group. Moreover, LY294002 was found to offset the advantages of IPO. To the best of our knowledge, this study provided the clear evidence to show that IPO significantly reduced the injury caused by I/R, and it might protect the liver from hepatic injury through activating the phosphoinositide 3-kinase pathway, which increased the expression of Akt, and inhibited the protein expression of IL-1, NF-κB-P65 and TNF-α.