Troxerutin alleviates hepatorenal toxicity induced by carbon tetrachloride in male mice.

OBJECTIVES

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, CCL4, CCL + TRX 75 mg/kg, CCL + TRX 150 mg/kg. Animals received oral TRX (75 and 150 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-2, cleaved caspase-3, 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

CCl caused a significant increase in the concentrations of liver and kidney indices such as ALT (<0.05), Cr (<0.01), AST (<0.001), and BUN (<0.001). Furthermore, CCl significantly increased the MDA level in the liver (<0.01) and kidney (<0.001) 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 CCl-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.