Abstract
This study investigated the possible roles of arginine (Arg) in ameliorating oxidative damage of intralipid (IL)-induced steatohepatitis (NASH).
NASH was induced in Sprague-Dawley rats by intravenous administration of 20 % IL for three weeks and then rats were pre- and post-treated with intraperitoneal injection of Arg for two weeks. Several biochemical parameters (blood and hepatic lipid peroxidation, glutathione, glutathione peroxidase and superoxide dismutase, hepatic cytochrome P450 2El monooxygenase (CYP2E1), nitric oxide (NO), endothelial nitric oxide synthase (eNOS) and tumor necrosis factor-α "TNF-α") and liver histopathology were detected for rat groups.
The administration of Arg either before or after IL significantly ameliorated uncontrolled elevation of TBARS content, CYP2E1 activity (0.32 ± 0.01 or 0.3 ± 0.02 IU/mg) and TNF-α level. These effects were associated with a significant increase in the levels of glutathione, activities of antioxidant enzymes, NO level (1.649 ± 0.047 or 1.957 ± 0.073 μmol/g) and activity of hepatic eNOS (0.05 ± 0.002 or 0.056 ± 0.002 IU/mg) compared to the IL-treated rats. Moreover, the injection of Arg in NASH-induced rats showed normal hepatocytes, no steatosis and no bile duct proliferation but mild inflammation in the group which received IL after Arg.
These results proved that pre- and post-treatment with Arg blocked oxidative stress-induced NASH by inhibiting CYP2E1 activity, decreasing TNF- α level and restoration activities of eNOS and antioxidant enzymes as well as glutathione level. This antioxidant effect of Arg leads to reverse signs of liver pathology of NASH with amelioration of liver and kidney functions.