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Green tea extract (Camellia sinensis) fermented by Lactobacillus fermentum attenuates alcohol-induced liver damage.

Bioscience, biotechnology, and biochemistry (2012-12-12)
Jong Ho Park, Younghoon Kim, Sae Hun Kim
RESUMEN

Here, the impact of an extract derived from green tea (Camellia sinensis) and fermentation with Lactobacilli fermentum strain OCS19 was explored with acute alcohol-induced liver damage. The study employed the HepG2 hepatic cell line and an in vivo murine model of liver damage. L. fermentum-fermented green tea extract (FGTE) was found to possess pronounced alcohol metabolizing enzyme activity. It significantly enhanced the cell viability of HepG2 cells following of them exposure, to ethanol (p<0.05) as compared with an extract derived from Hovenia dulcis, a positive control that is known for its action as an alcohol antagonist. Our in vivo studies indicated that prior administration of FGTE to alcohol-exposed mice significantly prevented subsequent increases in blood alcohol concentration (p<0.05), in addition to the induction of serum alanine aminotransferase (ALT) and triglycerides (p<0.05). Furthermore, the activity of hepatic alcohol dehydrogenase (ADH) and its mRNA expression level both increased in the livers of mice treated with FGTE, similarly to the H. dulcis-treated group. Taken together, these results may suggest that green tea extract coupled with L. fermentum fermentation attenuates the risk of ethanol-induced liver damage.

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Sigma-Aldrich
Alcohol Dehydrogenase from Saccharomyces cerevisiae, ≥300 units/mg protein, lyophilized powder (contains buffer salts), Mw 141-151 kDa
Sigma-Aldrich
Alcohol Dehydrogenase from Saccharomyces cerevisiae, powder, ≥300 units/mg protein, mol wt ~141,000 (four subunits)
Sigma-Aldrich
Alcohol Dehydrogenase from Saccharomyces cerevisiae
Sigma-Aldrich
Alcohol Dehydrogenase equine, recombinant, expressed in E. coli, ≥0.5 U/mg