Abstract: Objective To explore the pathogenesis of ischemic preconditioning to warm ischemia reperfusion injury of hepatocytes in rats. Methods Ninety SD rats were randomly divided into three experimental groups: sham operation group （group A）, warm hepatic ischemia/reperfusion group（group B and group C）. Group C was given ischemic preconditioning treatment. Serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected 0 h, 2 h, 6 h, 12 h and 24 h after ischemia reperfusion injury. Levels of TNF- α and IL- 1β were tested detected by ELISA. Levels of malondialdehyde (MDA) and superoxide dismutase (SOD) of hepatocytes were detected at the same time points. Mitochondrial membrane potential was examined to assess ischemia reperfusion injury of hepatocytes in rats using chart of intensity of JC-1 in mitochondria. Results The serum levels of ALT, TNF-α, IL-1β, and MDA were significantly higher in hepatic warm ischemia reperfusion group and ischemic preconditioning group than those in sham operation group (P＜ 0.05). Values of prothrombin activity and cholinesterase were significantly lower in liver warm ischemia reperfusion group and ischemic preconditioning group than those of sham operation group (P＜ 0.05). The SOD level of liver was significantly lower in warm ischemia reperfusion group and ischemic preconditioning group than that in sham operation group. The indexes were better in ischemic preconditioning group than those of warm ischemia reperfusion group (P＜ 0.05). The mitochondrial membrane potential level of liver cells reached the lowest value 0 hours after ischemia and reperfusion, and then increased gradually within 24 hours (P＜ 0.05). And the level of mitochondrial membrane potential of liver cells was significantly higher in ischemic preconditioning group than that in warm ischemia reperfusion group (P＜ 0.05). Conclusion Ischemic preconditioning may play a protective role in warm ischemia- reperfusion injury in rats. Ischemic preconditioning may significantly decrease the levels of ALT, AST, TNF-α, IL-1β and MDA, and increase the SOD activity in hepatocytes. The damage of mitochondrial membrane potential is decreased after ischemic preconditioning, which might be the pathogenesis of ischemic preconditioning to warm ischemia reperfusion injury of hepatocytes in rats.

Key words: alanine transaminase, aspartate aminotransferases, reperfusion injury, oxidative stress, mitochondria, ischemic preconditioning