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Naringin abates adverse effects of cadmium‐mediated hepatotoxicity: An experimental study using HepG2 cells
Author(s) -
Rathi Visesh Kumar,
Das Shubhankar,
Parampalli Raghavendra Archana,
Rao Bola Sadashiva Satish
Publication year - 2017
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21915
Subject(s) - chemistry , propidium iodide , lipid peroxidation , glutathione , apoptosis , cytochrome c , biochemistry , superoxide dismutase , metallothionein , cadmium chloride , oxidative stress , pharmacology , catalase , cadmium , programmed cell death , biology , enzyme , organic chemistry , gene
Abstract This study investigated the protective potential of Naringin (NIN) against cadmium chloride (CdCl 2 ) mediated hepatotoxicity using human hepatocellular carcinoma (HepG2) cells. An optimal concentration of NIN (5 μM) was potent enough to confer cytoprotection against CdCl 2 (50 μM) 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 sub‐G 0 /G 1 and Annexin V‐FITC/propidium iodide positive cells (apoptotic). NIN pretreatment maintained the levels of protein thiol along with endogenous activities of Superoxide dismutase, Glutathione S‐transferase , and Catalase and lowered lipid peroxidation. Decreased Bax/Bcl2 ratio along with reduced Caspase 3 cleavage and Cytochrome c release indicated that NIN conditioning blocked mitochondrial‐mediated 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 CdCl 2 mediated cytotoxicity.