Basic Research
Copyright ©The Author(s) 2005. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 21, 2005; 11(31): 4788-4793
Published online Aug 21, 2005. doi: 10.3748/wjg.v11.i31.4788
Effect of IL-10 on the expression of HSC growth factors in hepatic fibrosis rat
Mei-Na Shi, Wei-Da Zheng, Li-Juan Zhang, Zhi-Xin Chen, Xiao-Zhong Wang
Mei-Na Shi, Wei-Da Zheng, Li-Juan Zhang, Zhi-Xin Chen, Xiao-Zhong Wang, Department of Gastroenterology, Union Hospital of Fujian Medical University, Fuzhou 350001, Fujian Province, China
Author contributions: All authors contributed equally to the work.
Supported by Technology and Science Foundation of Fujian Province, No. 2003 D05
Correspondence to: Xiao-Zhong Wang, Department of Gastroenterology, Union Hospital of Fujian Medical University, Fuzhou 350001, Fujian Province, China. drwangxz@pub6.fz.fj.cn
Telephone: +86-591-83357896-8482
Received: August 30, 2004
Revised: December 3, 2004
Accepted: December 8, 2004
Published online: August 21, 2005
Abstract

AIM: To study the effect of IL-10 on the expression of growth factors - transforming growth factor-β1 (TGF-β1), epidermal growth factor (EGF), hepatocyte growth factor (HGF)and platelet-derived growth factor (PDGF) of hepatic stellate cells (HSCs) of hepatic fibrosis rat and the anti-fibrogenic role of exogenous IL-10.

METHODS: Hepatic fibrosis was induced by CCl4 administration intra-peritoneally. Sixty clean male Sprague-Dawley (SD) rats were randomly divided into three groups: normal control group (GN, 8 rats), hepatic fibrosis model group (GC, 28 rats) and IL-10 treated group (GI, 24 rats). At the beginning of the 7th and 11th wk, rats in each group were routinely perfused with pronase E and type IV collag-enase through a portal vein catheter and the suspension obtained from the liver was spun by centrifugation with 11% Nycodenz density gradient to isolate HSCs. Histological examination was used to determine the degree of hepatic fibrosis. RT-PCR was employed to analyze mRNA expression from freshly isolated cells. Immunocytochemistry was performed to detect protein expression in primary cultured HSCs.

RESULTS: Rat hepatic fibrosis was developed with the increase of injection frequency of CCl4, and HSCs were successfully isolated. At the 7th and 11th wk, TGF-β1, EGF, and HGF mRNA in GC increased obviously compared with GN (P = 0.001/0.042, 0.001/0.001, 0.001/0.001) and GI (P = 0.001/0.007, 0.002/0.001, 0.001/0.001). For TGF-β1, no difference was observed between GI and GN. For EGF, mRNA level in GI increased compared with GN during the 7th wk (P = 0.005) and 11th wk (P = 0.049). For HGF, mRNA level in GI decreased compared with GN at the 7th wk (P = 0.001) and 11th wk (P = 0.021). Between these two time points, TGF-β1 expression at the 7th wk was higher than that of the 11th wk (P = 0.049), but for EGF, the former was lower than the latter (P = 0.022). As for PDGF mRNA, there was no significant difference between these groups, but difference seemed to exist in protein levels. Results by immunocytochemistry of TGF-β1 and EGF were paralleled with the above findings.

CONCLUSION: The expression of TGF-β1, EGF and HGF increased in HSC of hepatic fibrosis rat and decreased after treatment with IL-10. IL-10 plays an anti-fibrogenic role by suppressing growth factors expression.

Keywords: Hepatic fibrosis; Hepatic stellate cells; Interleukin-10; Transforming growth factor-β1; Epidermal growth factor; Hepatocyte growth factor; Platelet-derived growth factor