Quercetin attenuates cadmium-induced hepatotoxicity by suppressing oxidative stress and apoptosis in rat

Background: Cadmium (Cd) is considered a major industrial and environmental toxicant, threatening the health of aquatic organisms, plants, animals, and humans. Quercetin (Que) is a natural flavonoid with antioxidant properties. The purpose of this study was to investigate the role of the oxidative stress and apoptosis in Cdinduced hepatotoxicity and the protective effect of Que. Methodology: Thirty-six male SD rats were randomly divided into 6 groups: control group, 1 mg/kg Cd group, 2 mg/kg Cd group, 1 mg/kg Cd+Que group, 2 mg/kg Cd + Que group, and a Que group. After a feeding period of 28 days, serum and liver tissue samples were collected to evaluate liver function, oxidative stress levels, liver histology, and apoptosis. Results: Experimental results confirmed that compared with the control group, the body weights of the Cd group significantly decreased. Additionally, there was a tremendous increased in the levels of ALT, AST, and LDH, and a significant decreased in the activities of SOD, CAT, and GSH content, while the level of MDA increased. Pathological sections of the liver showed that Cd-induced rats had ruptured liver tissue cells, exposed nuclei, and disturbed arrangement of hepatocyte cords. Cd exposure decreased the mRNA and protein expression of Nrf2 and NQO1 while increased the mRNA and protein expression of Keap1, thereby inducing oxidative stress. Meanwhile, Cd exposure increased the mRNA and protein expressions of Cytc, caspase-9, caspase-3, and Bax, while decreased the expression of Bcl-2. Conversely, after Que addition of alleviated liver injury and oxidative stress induced by Cd and inhibited apoptosis. Conclusion: In conclusion, Que alleviates hepatic toxicity induced by Cd through suppression of oxidative stress and apoptosis.