Effects and the mechanism of HGF on the apoptosis of rat primary cultured hepatic stellate cells treated with platelet-derived growth factor.
- Author:
Xiao-qin ZHONG
1
;
Wei SHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Hepatic Stellate Cells; drug effects; metabolism; Hepatocyte Growth Factor; pharmacology; Male; Platelet-Derived Growth Factor; pharmacology; Proto-Oncogene Proteins c-sis; Rats; Rats, Sprague-Dawley; Transcription Factor RelA; metabolism
- From: Chinese Journal of Hepatology 2008;16(9):665-668
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the inhibitory effect of hepatocyte growth factor (HGF) on the apoptosis of rat primary cultured hepatic stellate cells treated with platelet-derived growth factor BB (PDGF-BB).
METHODSHepatic stellate cells were cultured and treated with PDGF-BB+HGF, HGF or nothing (controls). Apoptosis of these hepatic stellate cells was evaluated by AO/EB staining, TUNEL and flow cytometry. Expression level of P65 was observed with immunocytochemical staining; DNA-protein binding complex of NF-kappa B was detected by electrophoretic mobility shift assay.
RESULTSThe cell apoptosis rate of the control group was lower than that of the PDGF-BB+HGF group. The apoptosis rate of the PDGF-BB+HGF group was lower than that of the HGF treated group; the expression of P65 was lower in the PDGF-BB+HGF group and HGF treated group compared to the normal control group; DNA-protein binding activity of NF-kappa B was respectively attenuated in the normal control group, PDGF-BB+HGF treated group and HGF treated group (P less than 0.05).
CONCLUSIONHGF can induce HSC apoptosis. Its possible mechanism may involve inhibiting DNA-protein binding activity of NF-kappa B and down-regulating the expression level of P65.
