Effects of salvianolic acid B on signal transduction induced by transforming growth factor-beta1 and platelet-derived growth factor- BB in hepatic stellate cells of rats.
- Author:
Dong-ying XUE
1
;
Jia-he HONG
;
Lie-ming XU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Benzofurans; pharmacology; Cells, Cultured; Hepatocytes; cytology; metabolism; Male; Mitogen-Activated Protein Kinase 1; metabolism; Mitogen-Activated Protein Kinase 3; metabolism; Platelet-Derived Growth Factor; biosynthesis; genetics; Proto-Oncogene Proteins c-sis; Rats; Rats, Sprague-Dawley; Signal Transduction; Transforming Growth Factor beta; biosynthesis; genetics
- From: Chinese Journal of Integrated Traditional and Western Medicine 2006;26(5):439-442
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the anti-hepatic fibrosis mechanisms of salvianolic acid B (SA-B).
METHODSHepatic stellate cells (HSCs) isolated from rats were primarily cultured in uncoated plastic culture dish for 7 days, then were incubated with 10(-6) mmol/L SA-B and stimulated with 10 ng/ml transforming growth factor-beta1 (TGF-beta1) or platelet-derived growth factor-BB (PDGF-BB). Expressions of extracellular-regulated kinase (ERK) and its phosphorylation in HSC, and expressions of TGF beta1, receptor I (TbetaR I) and II (TbetaR II) and PDGF receptor beta (PDGFR-beta) on the surface of HSC induced by TGF-beta1 or PDGF-BB were detected with Western blot assay.
RESULTSSA-B inhibited the phosphorylation of ERK1/2 in HSC primary normally cultivated for 9 days stimulated or un-stimulated by TGF-beta1, but could not affect the expressions of TbetaR I and TbetaR II on the HSC surface; it down-regulated the expression of PDGFR-beta, but had no obvious effect on the phosphorylation of ERK1/2 in those HSC stimulated or un-stimulated by PDGF-BB.
CONCLUSIONSA-B inhibits the ERK signal transduction induced by TGF-beta1 in HSC, which is independent of the expressions of TbetaR on HSC surface and also free from the ERK signal transduction stimulated by PDGF-BB. And its inhibition on PDGF-BB signal transduction in HSC is by way of restraining the expression of PDGFR in HSC.
