RESUMO
Cadmium (Cd) is one of the potent occupational and environmental toxicants, which induces oxidative stress to the multiple organs of the body, including liver. The present investigation was planned to evaluate the protective role of vitexin against Cd-prompted hepatotoxicity in rats. 24 male rats were divided into 4 groups viz. control, Cd-induced group (5 mg/kg), Cd + vitexin-treated group (2 mg/kg + 30 mg/kg), and vitexin-treated group (30 mg/kg). After 30 days of treatment, it was indicated that Cd escalated the level of liver function enzymes namely alanine transaminase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) as well as total bilirubin. Whereas the levels of albumin and total proteins were decreased in the rats. Additionally, it reduced the enzymatic activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GSR) and glutathione-S-transferase (GST), in addition to glutathione (GSH) content, whereas levels of malondialdehyde (MDA) and reactive oxygen species (ROS) were escalated. Furthermore, level of nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1ß) and interleukin-6 (IL-6) as well as the activity of cyclooxygenase-2 (COX-2) were increased. Besides, the level of Bax, caspase-9 and caspase-3 were elevated, while the Bcl-2 level was reduced following the Cd intoxication. Histopathological observation revealed significant hepatic tissue damage in Cd-administered rats. However, treatment of rats with vitexin significantly (p < 0.05) improved the Cd-induced disruptions in biochemical parameters as well as histological damages. Therefore, it is concluded that vitexin could be used as a therapeutic agent to counter the Cd-generated hepatic toxicity in rats owing to its anti-oxidant, anti-apoptotic and anti-inflammatory potential.