Improvement of 2,2′-Azobis(2-Methylpropionamidine) Dihydrochloride-Induced Hepatic Redox Imbalance in Swiss Mice and HepG2 Cells by Rutin

Redox imbalance can lead to irreversible damages to biological functions. In this context, rutin stands out for its antioxidant potential. The objective of this study was to evaluate the acute and chronic effect of rutin on the hepatic redox imbalance. The study was performed according to three different protocols. First, healthy male Swiss mice were divided into two groups: control and rutin, the second of which received chronic oral supplementation of rutin (10 mg/kg). The second involved evaluation of the generation of reactive oxygen species (ROS) by HepG2 cells, incubated or not with rutin (20 and 40 mu g/mL) for 3 h. The final protocol involved assessment of the acute effect of rutin (10 mg/kg) in mice with oxidative stress induced by 2,2 '-azobis(2-methylpropionamidine) dihydrochloride (ABAP). After the in vivo treatments, the livers were collected to analyze the oxidative damage by thiol, and the antioxidant defense by catalase, superoxide dismutase, and glutathione peroxidase. In the HepG2 cells, the following probes were employed to assess the ROS production: dichlorofluorescein, MitoSOX, dihydroethidium, and Amplex Red. Rutin administered chronically improved the antioxidant defense in healthy animals, and when administered acutely both inhibited the increased production of ROS in HepG2 cells and improved the redox imbalance parameters in mice with induced oxidative stress. This study suggests rutin as a protective agent for restoration of hepatic redox homeostasis in redox injury induced by ABAP in Swiss mice and HelpG2 cells.