The effects of Chinese national medicine of Huoxueruanjian compound on SMAD signal in hepatic stellate cell and its significance.
- Author:
Guo ZHANG
1
;
Fa-can ZHANG
;
Tian-cai WANG
;
Kuo-huan LIANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Collagen Type I; genetics; DNA-Binding Proteins; genetics; Liver Cirrhosis; drug therapy; etiology; pathology; Medicine, Chinese Traditional; RNA, Messenger; analysis; Rats; Smad3 Protein; Smad7 Protein; Trans-Activators; genetics
- From: Chinese Journal of Hepatology 2004;12(4):213-215
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEIn order to explore the roles of Huoxueruanjian compound on liver fibrogenesis and its molecular mechanism, this paper has investigated the Influence of blood serum with such traditional Chinese medicine compound on the expression of Smad3, Smad7 and procollagen alpha2(I) gene in hepatic stellate cell (HSC).
METHODSHSC-T6 was deal with different Concentration of blood serum medicine with Heluoshugan which was made by routine way. Then expression change of Smad3, Smad7 and procollagen alpha2(I) mRNA among each groups were observed by RT-PCR. Furthermore, the expression change of Smad3 protein were examined by Western blot.
RESULTSExpression of Smad3 and procollagen alpha2(I) mRNA as well as Smad3 protein had been downregulated after treating with blood serum medicine of Heluoshugan (P<0.01, P<0.05, respectively). The expression of procollagen alpha2(I) mRNA changed at the same tendency as those of Smad3. The role of blood serum medicine was significant difference between different concentration, P<0.05. And the expression of procollagen alpha2(I) mRNA changed in concentration-dependent manner. Blood serum medicine has no effects on the Smad7 mRNA.
CONCLUSIONThe anti-fibrosis roles of HuoXueruanjian Compound maybe influence the function of TGF-beta and Smad by nonspecific action, thereby inhibit the transcription of procollegan alpha2(I) mRNA and decrease the production of ECM. As regards Smad3, it may be facilitating the development of liver fibrosis when its expression increases. Otherwise, it manifest with anti-fibrosis role.