Basic Research
Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Mar 7, 2006; 12(9): 1386-1391
Published online Mar 7, 2006. doi: 10.3748/wjg.v12.i9.1386
Therapeutic effect of interleukin-10 on CCl4-induced hepatic fibrosis in rats
Yue-Hong Huang, Mei-Na Shi, Wei-Da Zheng, Li-Juan Zhang, Zhi-Xin Chen, Xiao-Zhong Wang
Yue-Hong Huang, 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
Supported by Nature Science Foundation of Fujian Province. No.2005D094 and No.C0410025
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: September 14, 2005
Revised: October 1, 2005
Accepted: October 26, 2005
Published online: March 7, 2006
Abstract

AIM: To study the therapeutic effect of exogenous interleukin-10 on CCl4-induced hepatic fibrosis in rats and its possible mechanisms.

METHODS: Fourty-seven SD rats were randomly divided into control group (group N) and CCl4-induced hepatic fibrosis model group (group C). After CCl4 was given for 9 wk, the model group was divided into three groups. Rats in group M were put to death immediately, rats in group T were treated with IL-10 for another three wk and then put to death, rats in group R recovered after three weeks and were then killed. The degree of hepatic fibrosis was measured by HE staining and histological activity index (HAI). Histological activity index (HAI), change of collagen types I and III were measured by Picrosirius staining. The expression of TNF-α, MMP-2 and TIMP-1 in liver tissue was measured by S-P immunohistochemistry.

RESULTS: CCl4- induced experimental rat hepatic fibrosis model was established successfully. The degree of hepatic fibrosis was markedly lower in group T than in groups M and R, and there was no difference between the two groups. The expression of collagen types I and III was significantly suppressed in group T and was slightly suppressed in groups M and R. The positive levels of TNF-α, MMP-2 and TIMP-1 in group M increased significantly compared to those in group N (P < 0.01). The positive signals decreased significantly in groups T and R (P < 0.01), but positive score was significantly lower in group T than in group R (P < 0.01).

CONCLUSION: Exogenous IL-10 can reverse CCl4-induced hepatic fibrosis in rats. IL-10 may exert its reversible effects on hepatic fibrosis by blocking CCl4-induced inflammation, inhibiting expression of MMP-2 and TIMP-1 and promoting resolution of collagen types I and III.

Keywords: Rat; Hepatic fibrosis; Interleukin-10; Tumor necrosis factor; Matrix metalloproteinase;Collagen