Isoliquiritigenin inhibits cell proliferation by a heme oxygenase-dependent pathway in rat hepatic stellate cells.

We evaluated whether the antiproliferative effects of isoliquiritigenin (ISL) on rat hepatic stellate cells (HSCs) are related to the induction of heme oxygenase 1 (HO-1) expression. ISL significantly inhibited serum- or growth factor-induced HSC proliferation. The inhibition of platelet-derived growth factor (PDGF)-induced proliferation by ISL was associated with the mitogen-activated protein kinase and phosphatidylinositol 3-kinase-Akt-p70 (S6K) pathways.

Gene expression profiles during the activation of rat hepatic stellate cells evaluated by cDNA microarray.

Hepatic stellate cells (HSCs) are activated by producing potentially injurious connective tissue components during hepatic fibrosis, thereby exerting a pivotal action in the development of liver fibrogenesis. The aim of this study was to investigate differences in gene expression patterns during the activation of HSCs using complementary cDNA microarrays. HSCs were isolated from normal rat livers and cultured for 0 (3 h), 3, 5 and 7 d.

2',4',6'-Tris(methoxymethoxy) chalcone attenuates hepatic stellate cell proliferation by a heme oxygenase-dependent pathway.

Proliferation of hepatic stellate cells (HSCs) is central for the development of fibrosis during liver injury. We have shown previously that butein (3,4,2',4'-tetrahydroxychalcone) suppresses myofibroblastic differentiation of rat HSCs. Our aim in this study was to determine whether a new synthetic chalcone derivative, 2',4',6'-tris(methoxymethoxy) chalcone (TMMC) inhibits HSC proliferation induced by serum- or platelet-derived growth factor (PDGF).

Tetrandrine induces apoptosis in hepatic stellate cells.

We have previously reported that tetrandrine reduced hepatic stellate cell activation and collagen accumulation in liver fibrosis induced by biliary obstruction. In the present study, we examined the apoptosis-inducing effect of tetrandrine on activated hepatic stellate cells, as the therapeutic goal in hepatic fibrosis is to eliminate the activated hepatic stellate cells by apoptosis. We used rat hepatic stellate cells transformed by Simian virus 40 (T-HSC/Cl-6) to overcome the limitations inherent in studying primary cultures of hepatic stellate cells.

The chalcone butein from Rhus verniciflua shows antifibrogenic activity.

Butein is known to be the major component of the bark of Rhus verniciflua Stokes (Anacardiaceae). The aim of this work was to investigate the effects of butein on liver fibrosis induced by carbon tetrachloride (CCl4) in rats, and to explore its antifibrogenic mechanism. Butein (10 mg/kg/day or 25 mg/kg/day) showed a significant reduction of hydroxyproline and malondialdehyde levels in rats.

Butein suppresses myofibroblastic differentiation of rat hepatic stellate cells in primary culture.

Hepatic stellate cells play a key role in the pathogenesis of hepatic fibrosis. In this study, we investigate the inhibitory effect of butein on the activation and proliferation of rat primary cultured hepatic stellate cells. Possible cytotoxic effects were measured on stellate cells and hepatocytes using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.

Aloe emodin suppresses myofibroblastic differentiation of rat hepatic stellate cells in primary culture.

We have studied the inhibitory effect of aloe emodin on hepatic stellate cells activation and proliferation, as these cells play a key role in the pathogenesis of hepatic fibrosis. Rat hepatic stellate cells were activated by contact with plastic dishes, resulting in their transformation into myofibroblast-like cells. Primary hepatic stellate cells were exposed to aloe emodin (1-10 microg/ml).

Curcumin inhibits collagen synthesis and hepatic stellate cell activation in-vivo and in-vitro.

We previously demonstrated that curcumin, a well-known antioxidant, inhibits collagen deposition in carbon tetrachloride-induced liver injury in rats. The major effector cells responsibleforcollagensynthesis in the liver are activated hepatic stellate cells. In this study,we investigated the inhibitory effects of curcumin on the collagen synthesis and activation of rat hepatic stellate cells in-vitro, and on hepatic stellate cell activation in-vivo.