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Epigallocatechin‐3‐gallate(‐)Protects Chang Liver Cells against Ethanol‐Induced Cytotoxicity and Apoptosis
Author(s) -
Kaviarasan Subramanian,
Ramamurthy Nalini,
Gunasekaran Palani,
Varalakshmi Elango,
Anuradha Carani V.
Publication year - 2007
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2006.00036.x
Subject(s) - glutathione , lactate dehydrogenase , lipid peroxidation , chemistry , cytotoxicity , apoptosis , reactive oxygen species , biochemistry , propyl gallate , oxidative stress , glutathione disulfide , antioxidant , pharmacology , biology , in vitro , enzyme
The objective of the study was to investigate the effect of epigallocatechin‐3‐gallate (EGCG) on ethanol (EtOH)‐induced cytotoxicity in human Chang liver cells. Cells were incubated with either 30 mM EtOH alone or together in presence of (25 µM) EGCG for 24 hr. Assays were performed in treated cells to evaluate the ability of EGCG to prevent the toxic effects of EtOH. EtOH exposure suppressed the growth of Chang liver cells and induced lactate dehydrogenase leakage, oxygen radical formation, peroxidation of lipids, mitochondrial dysfunction and apoptosis. Reduced glutathione (GSH) concentration was significantly decreased ( P < 0.05) while oxidized glutathione (GSSG) concentration was significantly elevated in EtOH‐treated cells as compared to normal cells. Incubation of EGCG along with EtOH significantly prevented EtOH‐dependent cell loss and lactate dehydrogenase leakage. This was associated with a reduction in oxidative damage as reflected by a reduction in the generation of reactive oxygen species, and in lipid peroxidation and maintenance of intracellular GSH/GSSG ratio. EGCG decreased the accumulation of sub‐G 1 phase cells and reduced apoptosis. The findings suggest that EGCG exerts a protective action during EtOH‐induced liver cell damage.