Abstract

The aim of study is to detect the effects and relevant mechanisms of oxysophoridine on alcoholic hepatic injury in mice. Sixty male Institute of Cancer Research (ICR) mice were randomly divided into a normal control group, an alcoholic liver injury model group, a positive control (tiopronin) group and an oxysophoridine (250, 125, 62.5 mg/kg) group. Consecutive interventions were conducted on each group for 10 days; specimens were obtained according to requirements of the testing indicators 16 h after the last drug administration. The protective effects were evaluated by biochemical parameters including serum aspartate transaminase (AST), alanine transferase (ALT), reduced glutathione (GPx), liver malondialdehyde (MDA) and superoxide dismutase (SOD). The pathological changes of the liver in microstructure and ultrastructure were observed. A decreased level of serum ALT, AST activity and liver MDA content with increased liver SOD, GPx activity (P<0.05) were observed (P<0.05) in the oxysophoridine group compared with the alcoholic liver injury model group, in which elevated serum ALT and AST activity were recorded, along with a marked increase of liver MDA (P<0.05), decrease of liver SOD and GPx (P<0.05). The following changes of the liver were observed in the model group: Blurred contour of the hepatic lobule with punctated or focal necrosis in partial liver cells, multiple intracellular microvesicular steatosis, with lipid droplets formed in the cytoplasm, marked swelling of hepatocytes and disarrangement of hepatic cords, swelling of mitochondria, with disappeared or broken cristae, enlarged endoplasmic reticulum and condensed chromatin. Compared with the model group, a decrease in pathological changes of various degrees was observed in the oxysophoridine group at various doses. The result indicates that oxysophoridine prevents alcoholic liver damage in mice and the protective effect may be associated with anti-oxidative stress.

Key words:  Alcohol, oxysophoridine, oxidative stress, antioxidants.