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.
Highlights
Alcohol-related liver disease (ALD) is a major public health hazard in developed as well as in developing world (Abdul et al, 2010)
Alanine transferase (ALT), aspartate transaminase (AST), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) kits were purchased from Jiancheng Bioengineering Institute (Nanjing)
Administration of OSR to alcohol treated mice significantly (P < 0.05) increased the activities of enzymatic antioxidants when compared to alcohol treated mice
Summary
Alcohol-related liver disease (ALD) is a major public health hazard in developed as well as in developing world (Abdul et al, 2010). Upwards to 90% of individuals consuming alcohol on a daily basis develop fatty liver (steatosis) which can resolve upon cessation of alcohol consumption (Smathers et al, 2011). Alcohol abuse remains one of the most common causes of acute and chronic liver diseases in the world. Alcohol remains one of the most common causes of both acute and chronic liver disease in the United States (Sofair et al, 2010). In Western countries, up to 50% of cases of end-stage liver disease have alcohol as a major etiologic factor (Orholm et al, 1985)
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