Epigallocatechin gallate enhances biliary cholesterol secretion in healthy rats and lowers plasma and liver cholesterol in ethinylestradiol-treated rats
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
22771784
DOI
10.1016/j.ejphar.2012.06.034
PII: S0014-2999(12)00546-8
Knihovny.cz E-resources
- MeSH
- Biological Transport drug effects genetics MeSH
- Cholesterol blood metabolism MeSH
- Ethinyl Estradiol pharmacology MeSH
- Phospholipids metabolism MeSH
- Intestinal Absorption drug effects MeSH
- Liver drug effects metabolism MeSH
- Catechin analogs & derivatives pharmacology MeSH
- Rats MeSH
- Rats, Wistar MeSH
- Gene Expression Regulation drug effects MeSH
- Health * MeSH
- Biliary Tract drug effects metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Cholesterol MeSH
- epigallocatechin gallate MeSH Browser
- Ethinyl Estradiol MeSH
- Phospholipids MeSH
- Catechin MeSH
The beneficial effect of the major green tea catechin, epigallocatechin gallate (EGCG), on cholesterol homeostasis has been studied mainly in relation to the intestinal absorption of cholesterol; however, how EGCG affects cholesterol metabolism in the liver is not entirely known. The present study investigated the effect of EGCG on liver cholesterol metabolism in healthy and ethinylestradiol-treated rats. EGCG treatment reduced plasma total cholesterol in ethinylestradiol-treated animals and very low density lipoprotein cholesterol in both groups receiving EGCG. In healthy rats, despite the decrease in bile flow, EGCG markedly enhanced biliary secretion of cholesterol and phospholipids. These changes were correlated with increased expression of ATP-binding cassette transporter G5 and G8 and scavenger receptor class B type 1, and decreased expression of acyl-CoA:cholesterol acyltransferase. Ethinylestradiol treatment caused marked hepatic cholesterol accumulation with a concomitant liver weight increase and plasma cholesterol reduction. In ethinylestradiol-treated rats, EGCG co-administration attenuated the increase in liver cholesterol and liver weight. Furthermore, EGCG blunted induction of acyl-CoA:cholesterol acyltransferase and raised reduced levels of ATP-binding cassette transporter G5 and G8 and 3-hydroxy-3-methyl-glutaryl-CoA reductase in ethinylestradiol-treated rats. In conclusion, this study has demonstrated for the first time the ability of EGCG to enhance biliary cholesterol secretion and to attenuate ethinylestradiol-induced liver cholesterol accumulation. Changes in the expression of relevant enzymes and transporters suggest evidence of another mechanism that may contribute to the overall effect of EGCG on cholesterol metabolism and imply new physiological consequences of this widely used compound.
References provided by Crossref.org
In vitro toxicity of epigallocatechin gallate in rat liver mitochondria and hepatocytes