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Statements

Subject Item
n2:RIV%2F00216208%3A11160%2F13%3A10134414%21RIV14-GA0-11160___
rdf:type
n15:Vysledek skos:Concept
rdfs:seeAlso
http://www.sciencedirect.com/science/article/pii/S0300483X12003745
dcterms:description
Epigallocatechin gallate (EGCG) has been shown to be protective in various experimental models of liver injury, although opposite effects have also been reported. Since its effect on biliary physiology has not been thoroughly investigated, the present study evaluated effect of EGCG on bile flow and bile acid homeostasis in rats. Compared to controls, EGCG treatment decreased bile flow by 23%. Hepatic paracellular permeability and biliary bile acid excretion were not altered by EGCG administration, but biliary glutathione excretion was reduced by 70%. Accordingly, the main glutathione transporter on the hepatocyte canalicular membrane, multidrug resistance-associated protein 2 (Mrp2), was significantly decreased at the protein level. EGCG administration also doubled plasma bile acid levels compared to controls. While protein levels of the main hepatic bile acid transporters were unchanged, the rate-limiting enzyme in the bile acid synthesis, Cyp7a1, was significantly increased by EGCG. Enhanced bile acid synthesis in these animals was also confirmed by a 2-fold increase in plasma marker 7 alpha-hydroxy-4-cholesten-3-one. In contrast, EGCG markedly downregulated major bile acid transporters (Asbt and Ost alpha) and regulatory molecules (Shp and Fgf15) in the ileum. When EGCG was coadministered with ethinylestradiol, a potent cholestatic agent, it did not show any additional effect on the induced cholestasis. This study shows ability of EGCG to raise plasma bile acid concentrations, mainly through Cyp7a1 upregulation, and to decrease bile production through reduction in Mrp2-mediated bile acid-independent bile flow. In conclusion, our data demonstrate that under certain conditions EGCG may induce cholestasis. Epigallocatechin gallate (EGCG) has been shown to be protective in various experimental models of liver injury, although opposite effects have also been reported. Since its effect on biliary physiology has not been thoroughly investigated, the present study evaluated effect of EGCG on bile flow and bile acid homeostasis in rats. Compared to controls, EGCG treatment decreased bile flow by 23%. Hepatic paracellular permeability and biliary bile acid excretion were not altered by EGCG administration, but biliary glutathione excretion was reduced by 70%. Accordingly, the main glutathione transporter on the hepatocyte canalicular membrane, multidrug resistance-associated protein 2 (Mrp2), was significantly decreased at the protein level. EGCG administration also doubled plasma bile acid levels compared to controls. While protein levels of the main hepatic bile acid transporters were unchanged, the rate-limiting enzyme in the bile acid synthesis, Cyp7a1, was significantly increased by EGCG. Enhanced bile acid synthesis in these animals was also confirmed by a 2-fold increase in plasma marker 7 alpha-hydroxy-4-cholesten-3-one. In contrast, EGCG markedly downregulated major bile acid transporters (Asbt and Ost alpha) and regulatory molecules (Shp and Fgf15) in the ileum. When EGCG was coadministered with ethinylestradiol, a potent cholestatic agent, it did not show any additional effect on the induced cholestasis. This study shows ability of EGCG to raise plasma bile acid concentrations, mainly through Cyp7a1 upregulation, and to decrease bile production through reduction in Mrp2-mediated bile acid-independent bile flow. In conclusion, our data demonstrate that under certain conditions EGCG may induce cholestasis.
dcterms:title
Cholestatic effect of epigallocatechin gallate in rats is mediated via decreased expression of Mrp2 Cholestatic effect of epigallocatechin gallate in rats is mediated via decreased expression of Mrp2
skos:prefLabel
Cholestatic effect of epigallocatechin gallate in rats is mediated via decreased expression of Mrp2 Cholestatic effect of epigallocatechin gallate in rats is mediated via decreased expression of Mrp2
skos:notation
RIV/00216208:11160/13:10134414!RIV14-GA0-11160___
n15:predkladatel
n19:orjk%3A11160
n3:aktivita
n16:S n16:P n16:I
n3:aktivity
I, P(GBP303/12/G163), S
n3:cisloPeriodika
1
n3:dodaniDat
n6:2014
n3:domaciTvurceVysledku
n11:8502250 n11:4835549
n3:druhVysledku
n14:J
n3:duvernostUdaju
n13:S
n3:entitaPredkladatele
n12:predkladatel
n3:idSjednocenehoVysledku
65333
n3:idVysledku
RIV/00216208:11160/13:10134414
n3:jazykVysledku
n20:eng
n3:klicovaSlova
bile acids; cholestasis; bile formation; epigallocatechin gallate
n3:klicoveSlovo
n4:cholestasis n4:bile%20acids n4:epigallocatechin%20gallate n4:bile%20formation
n3:kodStatuVydavatele
NL - Nizozemsko
n3:kontrolniKodProRIV
[EB4951B9582A]
n3:nazevZdroje
Toxicology
n3:obor
n10:FR
n3:pocetDomacichTvurcuVysledku
2
n3:pocetTvurcuVysledku
15
n3:projekt
n8:GBP303%2F12%2FG163
n3:rokUplatneniVysledku
n6:2013
n3:svazekPeriodika
303
n3:tvurceVysledku
Tomšík, Pavel Leníček, Martin Hiršová, Petra Kučera, Otto Mičuda, Stanislav Červinková, Zuzana Hroch, Miloš Vítek, Libor Pávek, Petr Karlasová, Gabriela Šišpera, Luděk Doleželová, Eva Zagórová, Marie Cermanová, Jolana Kadová, Zuzana
n3:wos
000314856800002
s:issn
0300-483X
s:numberOfPages
7
n21:doi
10.1016/j.tox.2012.10.018
n9:organizacniJednotka
11160