Troxerutin alleviates hepatorenal toxicity induced by carbon tetrachloride in male mice

Objective(s): Troxerutin (TRX) is a natural bioflavonoid with several medicinal properties. We assessed its protective effect on carbon tetrachloride-related hepatorenal damage in male mice.Materials and Methods: Male mice were assigned to five groups: Control, TRX, CCL۴, CCL۴ + TRX ۷۵ mg/kg, CCL۴ + TRX ۱۵۰ mg/kg. Animals received oral TRX (۷۵ and ۱۵۰ mg/kg) daily for four weeks. After treatments, serum liver enzymes aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Serum blood urine nitrogen (BUN), and creatinine (Cr) levels were assessed. Malondialdehyde (MDA, the primary lipid peroxidation product), activity of anti-oxidant enzymes glutathione peroxidase (GPX), superoxide dismutase (SOD), and total anti-oxidant capacity (TAC) were determined. Using the immunoblotting method, Bax, Bcl-۲, cleaved caspase-۳, and cytochrome-c protein concentrations were evaluated in the kidney and liver tissues. The Hematoxylin and Eosin (H&E) staining were used to assess the kidney and liver histopathological changes.Results: CCl۴ caused a significant increase in the concentrations of liver and kidney indices such as ALT (P<۰.۰۵), Cr (P<۰.۰۱), AST (P<۰.۰۰۱), and BUN (P<۰.۰۰۱). Furthermore, CCl۴ significantly increased the MDA level in the liver (P<۰.۰۱) and kidney (P<۰.۰۰۱) tissues while decreasing anti-oxidant status. TRX could significantly decrease ALT, AST, Cr, BUN, and MDA concentrations and increase SOD, GPx, and TAC activities in comparison to the CCl۴-damaged control group. In addition, TRX caused an attenuation in the pro and anti-apoptotic markers in the kidney and liver tissues. Conclusion: TRX displayed liver and kidney protection, possibly by its free radical scavenging and anti-oxidant effects.

کلیدواژه ها:

Apoptosis ، Carbon tetrachloride ، Mice ، Oxidative stress ، Troxerutin