Fructose-1,6-bisphosphate induces phenotypic reversion of activated hepatic stellate cell

被引：17

作者：

de Mesquita, Fernanda C. ^{[1
]}

Bitencourt, Shanna ^{[1
]}

Caberlon, Eduardo ^{[1
]}

da Silva, Gabriela V. ^{[1
]}

Basso, Bruno S. ^{[1
]}

Schmid, Julia ^{[1
]}

Ferreira, Gabriela A. ^{[1
]}

de Oliveira, Fernanda dos Santos ^{[2
]}

de Oliveira, Jarbas R. ^{[1
]}

机构：

[1] Pontificia Univ Catolica Rio Grande do Sul, Lab Pesquisa Biofis Celular & Inflamacao, Porto Alegre, RS, Brazil

[2] Hosp Clin Porto Alegre Res Ctr, Porto Alegre, RS, Brazil

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2013年 / 720卷 / 1-3期

关键词：

Fructose-16-bisphosphate; Hepatic stellate cell; Fibrosis; Peroxisome proliferator-activated receptor gamma; Transforming growth factor-beta; PPAR-GAMMA EXPRESSION; LIPOCYTE PHENOTYPE; TGF-BETA; INDUCTION; FIBROSIS; LINE; CONVERSION; PROLIFERATION; GALACTOSAMINE; METABOLISM;

D O I：

10.1016/j.ejphar.2013.09.067

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

Hepatic stellate cells (HSC) play a key role in liver fibrogenesis. Activation of PPAR gamma and inhibition of fibrogenic molecules are potential strategies to block HSC activation and differentiation. Aware that the process of hepatic fibrosis involves inflammatory mediators, various anti-inflammatory substances have been studied in an attempt to revert fibrosis. The purpose of this study was to investigate the in vitro effects of fructose-1,6-bisphosphate (FBP) on HSC phenotype reversion. The results demonstrated that FBP induced quiescent phenotype in GRX cells via PPAR gamma activation. Significant decrease in type I collagen mRNA expression was observed in the first 24 h of treatment. These events preceded the reduction of TGF-beta 1 and total collagen secretion. Thus, FBP promoted downregulation of HSC activation by its antifibrotic action. These findings demonstrate that FBP may have potential as a novel therapeutic agent for the treatment of liver fibrosis. (C) 2013 Elsevier B.V. All rights reserved.

引用

页码：320 / 325

页数：6

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