[Effect of genistein on hepatic stellate cell proliferation and lipid peroxidation in vitro].

Objective: To investigate the effect of genistein on the proliferation and lipid peroxidation of hepatic stellate cells (HSC) in vitro and its the protective effect against hepatic fibrosis.

Methods: Rat hepatic stellate cells (HSC-T6 cells) were divided into 3 groups and incubated in the presence of 0.1 mol/L hydrogen dioxide followed by washing with PBS for 3 times.

The binding sites for the chromatin insulator protein CTCF map to DNA methylation-free domains genome-wide.

All known vertebrate chromatin insulators interact with the highly conserved, multivalent 11-zinc finger nuclear factor CTCF to demarcate expression domains by blocking enhancer or silencer signals in a position-dependent manner. Recent observations document that the properties of CTCF include reading and propagating the epigenetic state of the differentially methylated H19 imprinting control region. To assess whether these findings may reflect a universal role for CTCF targets, we identified more than 200 new CTCF target sites by generating DNA microarrays of clones derived from chromatin-immunopurified (ChIP) DNA followed by ChIP-on-chip hybridization analysis.

Effects of estradiol on liver estrogen receptor-alpha and its mRNA expression in hepatic fibrosis in rats.

Aim: Estradiol treatment regulates estrogen receptor (ER) level in normal rat liver. However, little information is available concerning the role of estrogen in regulating liver ER in hepatic fibrosis in rats. The present study was conducted to determine whether estradiol treatment in CCl4-induced liver fibrosis of female and ovariectomized rats altered liver ERalpha and its mRNA expression, and to investigate the possible mechanisms.

Estrogen reduces CCL4- induced liver fibrosis in rats.

Aim: Chronic liver diseases, such as fibrosis or cirrhosis, are more common in men than in women. This gender difference may be related to the effects of sex hormones on the liver. The aim of the present work was to investigate the effects of estrogen on CCL(4)-induced fibrosis of the liver in rats.