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

## TL;DR

Troxerutin helps protect the liver and kidneys of male mice from damage caused by carbon tetrachloride, likely through its antioxidant properties.

## Contribution

This study demonstrates the hepatorenal protective effects of Troxerutin against carbon tetrachloride-induced toxicity in mice.

## Key findings

- Troxerutin reduced elevated liver and kidney damage markers like ALT, AST, Cr, and BUN caused by CCl4.
- Troxerutin increased antioxidant enzyme activities (SOD, GPx, TAC) and reduced lipid peroxidation (MDA) in liver and kidney tissues.
- Troxerutin attenuated pro-apoptotic and anti-apoptotic protein levels in liver and kidney tissues.

## Abstract

Troxerutin (TRX) is a natural bioflavonoid with several medicinal properties. We assessed its protective effect on carbon tetrachloride-related hepatorenal damage in male mice.

Male mice were assigned to five groups: Control, TRX, CCL4, CCL4 + TRX 75 mg/kg, CCL4 + 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.

CCl4 caused a significant increase in the concentrations of liver and kidney indices such as ALT (P<0.05), Cr (P<0.01), AST (P<0.001), and BUN (P<0.001). Furthermore, CCl4 significantly increased the MDA level in the liver (P<0.01) and kidney (P<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 CCl4-damaged control group. In addition, TRX caused an attenuation in the pro and anti-apoptotic markers in the kidney and liver tissues.

TRX displayed liver and kidney protection, possibly by its free radical scavenging and anti-oxidant effects.