Abstract: Objective To explore the pathogenesis of oxidative stress damage to mitochondrial membrane and electrophysiological dysfunction of ischemia reperfusion injury of hepatocytes in rats. Methods Seventy rats were randomly divided into three experimental groups: sham operation (SHAM) group, warm hepatic ischemia/reperfusion (wI/R) group and cold hepatic ischemia/reperfusion (cI/R) group. Blood samples were collected for the detection of alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor- α (TNF-α) and interleukin (IL) -1 β levels. Bile samples were collected for the detection of glucose and γ-glutamyl transferase (GGT) levels. And liver samples were collected for the detection of malondialdehyde (MDA) and superoxide dismutase (SOD). Flow cytometry was used to detect mitochondrial membrane potential. The mitochondrial respiratory chain complex was examined using ELISA to assess ischemia reperfusion injury of hepatocytes in rats. Results The results indicated that ALT, AST, GLU, GGT, TNF-α, IL-1β and MDA levels were increased significantly in the wI/R group and cI/R group than those in SHAM group (P＜0.01), and those indexes were significantly higher in cI/R group than those of wI/R group (P＜0.05). The SOD level was significantly lower in wI/R group and cI/R group than that in SHAM group, which was significantly higher in wI/R group than that of cI/R group (P＜0.01). Compared with SHAM group, ratios of mitochondrial membrane potential were significantly decreased at 0, 1 and 12 h I/R in wI/R group and cI/R group (P＜0.01). The activity of mitochondrial membrane potential was gradually recovered with time in wI/R group and cI/R group (P＜0.01). There were no significant differences in mitochondrial respiratory chain complexes Ⅲ and Ⅳ between 0 h and 72 h in SHAM group. The activity of mitochondrial respiratory chain complexes was increased at 72 h than that of 0 h in wI/R group and cI/R group (P＜0.01). The activity of mitochondrial respiratory chain complexes Ⅲ was decreased ordinally at 0 h and 72 h, and the activity of mitochondrial respiratory chain complexes Ⅳ was increased ordinally in SHAM group, wI/R group and cI/R group (P＜0.01). Conclusion Mitochondrial membrane potential is significantly decreased after ischemia reperfusion injury, and the activity of mitochondrial respiratory chain complexes is significantly decreased as well, which might be the pathogenesis of oxidative stress damage to mitochondrial membrane and electrophysiological dysfunction of ischemia reperfusion injury of hepatocytes in rats.

Key words: liver transplantation, reperfusion injury, disease models, animal, oxidative stress, mitochondrial transmembrane potential, liver damage