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Statements

Subject Item
n2:RIV%2F00179906%3A_____%2F12%3A10123846%21RIV13-MZ0-00179906
rdf:type
skos:Concept n11:Vysledek
rdfs:seeAlso
http://www.sciencedirect.com/science/article/pii/S0014299912005468
dcterms:description
The present paper describes our investigation of the effect of epigallocatechin-gallate (EGCG), the major active ingredient from the green tea, on liver cholesterol metabolism in control and ethinylestradiol-treated rats. The results demonstrated that EGCG administration to control rats did not change plasma total cholesterol, but reduced VLDL cholesterol. However, EGCG markedly enhanced biliary cholesterol and phospholipid secretion, despite the decrease in bile flow and biliary bile acid secretion. In ethinylestradiol treated rats, EGCG caused reduction in hepatic cholesterol accumulation and consequently also mitigation of drug-induced hepatomegaly. These effect of EGCG were attributable to its inducing effect on protein expression of ATP-binding cassette transporter G5 and 8 (ABCG5/8) - i.e. cholesterol biliary exporter, and the reduced expression of acyl-CoA:cholesterol acyltransferase (ACAT2) protein - i.e. limiting step for cholesterol liver storage and VLDL production. Our data for the first time demonstrated these metabolic effect for such a commonly used substance. The present paper describes our investigation of the effect of epigallocatechin-gallate (EGCG), the major active ingredient from the green tea, on liver cholesterol metabolism in control and ethinylestradiol-treated rats. The results demonstrated that EGCG administration to control rats did not change plasma total cholesterol, but reduced VLDL cholesterol. However, EGCG markedly enhanced biliary cholesterol and phospholipid secretion, despite the decrease in bile flow and biliary bile acid secretion. In ethinylestradiol treated rats, EGCG caused reduction in hepatic cholesterol accumulation and consequently also mitigation of drug-induced hepatomegaly. These effect of EGCG were attributable to its inducing effect on protein expression of ATP-binding cassette transporter G5 and 8 (ABCG5/8) - i.e. cholesterol biliary exporter, and the reduced expression of acyl-CoA:cholesterol acyltransferase (ACAT2) protein - i.e. limiting step for cholesterol liver storage and VLDL production. Our data for the first time demonstrated these metabolic effect for such a commonly used substance.
dcterms:title
Epigallocatechin gallate enhances biliary cholesterol secretion in healthy rats and lowers plasma and liver cholesterol in ethinylestradiol-treated rats Epigallocatechin gallate enhances biliary cholesterol secretion in healthy rats and lowers plasma and liver cholesterol in ethinylestradiol-treated rats
skos:prefLabel
Epigallocatechin gallate enhances biliary cholesterol secretion in healthy rats and lowers plasma and liver cholesterol in ethinylestradiol-treated rats Epigallocatechin gallate enhances biliary cholesterol secretion in healthy rats and lowers plasma and liver cholesterol in ethinylestradiol-treated rats
skos:notation
RIV/00179906:_____/12:10123846!RIV13-MZ0-00179906
n11:predkladatel
n14:ico%3A00179906
n4:aktivita
n17:S n17:I
n4:aktivity
I, S
n4:cisloPeriodika
1-3
n4:dodaniDat
n15:2013
n4:domaciTvurceVysledku
n8:5930596
n4:druhVysledku
n19:J
n4:duvernostUdaju
n13:S
n4:entitaPredkladatele
n5:predkladatel
n4:idSjednocenehoVysledku
134602
n4:idVysledku
RIV/00179906:_____/12:10123846
n4:jazykVysledku
n6:eng
n4:klicovaSlova
ethinylestradiol; epigallocatechin gallate; biliary secretion; cholesterol metabolism
n4:klicoveSlovo
n10:cholesterol%20metabolism n10:biliary%20secretion n10:epigallocatechin%20gallate n10:ethinylestradiol
n4:kodStatuVydavatele
NL - Nizozemsko
n4:kontrolniKodProRIV
[711B76D7B33E]
n4:nazevZdroje
European Journal of Pharmacology
n4:obor
n12:FR
n4:pocetDomacichTvurcuVysledku
1
n4:pocetTvurcuVysledku
7
n4:rokUplatneniVysledku
n15:2012
n4:svazekPeriodika
691
n4:tvurceVysledku
Hiršová, Petra Cermanová, Jolana Mičuda, Stanislav Doleželová, Eva Kolouchová, Gabriela Hyšpler, Radomír Kadová, Zuzana
n4:wos
000307815800005
s:issn
0014-2999
s:numberOfPages
8
n18:doi
10.1016/j.ejphar.2012.06.034