Naringin abates adverse effects of cadmium‐mediated hepatotoxicity: An experimental study using HepG2 cells

摘要

Abstract This study investigated the protective potential of Naringin (NIN) against cadmium chloride (CdCl2 ) mediated hepatotoxicity using human hepatocellular carcinoma (HepG2) cells. An optimal concentration of NIN (5xM) was potent enough to confer cytoprotection against CdCl2 (50xM) as was observed by MTT assay. Preconditioning with NIN maintained redox homeostasis, mitochondrial membrane potential, and reduced apoptosis as marked by decrease in the percentage subG0 /G1 and Annexin VFITC/propidium iodide positive cells (apoptotic). NIN pretreatment maintained the levels of protein thiol along with endogenous activities ofSuperoxide dismutase, Glutathione Stransferase , andCatalase and lowered lipid peroxidation. Decreased Bax/Bcl2 ratio along with reduced Caspase 3 cleavage and Cytochromec release indicated that NIN conditioning blocked mitochondrialmediated apoptosis. Increased Nrf2 and metallothionein (MT) acted as adaptive response in the presence of cadmium. Thus, the protective mechanism of NIN is attributed to its antioxidant potential which aids in redox homeostasis and prevents CdCl2 mediated cytotoxicity.