TY - JOUR
T1 - Naringin abates adverse effects of cadmium-mediated hepatotoxicity
T2 - An experimental study using HepG2 cells
AU - Rathi, Visesh Kumar
AU - Das, Shubhankar
AU - Parampalli Raghavendra, Archana
AU - Rao, Bola Sadashiva Satish
N1 - Publisher Copyright:
© 2017 Wiley Periodicals, Inc.
PY - 2017/8/1
Y1 - 2017/8/1
N2 - 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 (5 μM) was potent enough to confer cytoprotection against CdCl2 (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-G0/G1 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 CdCl2 mediated cytotoxicity.
AB - 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 (5 μM) was potent enough to confer cytoprotection against CdCl2 (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-G0/G1 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 CdCl2 mediated cytotoxicity.
UR - https://www.scopus.com/pages/publications/85018572278
UR - https://www.scopus.com/pages/publications/85018572278#tab=citedBy
U2 - 10.1002/jbt.21915
DO - 10.1002/jbt.21915
M3 - Article
AN - SCOPUS:85018572278
SN - 1095-6670
VL - 31
JO - Journal of Biochemical and Molecular Toxicology
JF - Journal of Biochemical and Molecular Toxicology
IS - 8
M1 - e21915
ER -
