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

Visesh Kumar Rathi; Shubhankar Das; Archana Parampalli Raghavendra; Bola Sadashiva Satish Rao

doi:10.1002/jbt.21915

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

Visesh Kumar Rathi, Shubhankar Das, Archana Parampalli Raghavendra, Bola Sadashiva Satish Rao

Research output: Contribution to journal › Article › peer-review

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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 (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.

Original language	English
Article number	e21915
Journal	Journal of Biochemical and Molecular Toxicology
Volume	31
Issue number	8
DOIs	https://doi.org/10.1002/jbt.21915
Publication status	Published - 01-08-2017

All Science Journal Classification (ASJC) codes

Biochemistry
Molecular Medicine
Molecular Biology
Toxicology
Health, Toxicology and Mutagenesis

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1002/jbt.21915

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title = "Naringin abates adverse effects of cadmium-mediated hepatotoxicity: An experimental study using HepG2 cells",

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 (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.",

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AU - Das, Shubhankar

AU - Parampalli Raghavendra, Archana

AU - Rao, Bola Sadashiva Satish

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.

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

Abstract

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UN SDGs

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