Basic Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 1, 2004; 10(1): 77-81
Published online Jan 1, 2004. doi: 10.3748/wjg.v10.i1.77
Effects of cytokines on carbon tetrachloride-induced hepatic fibrogenesis in rats
Li-Juan Zhang, Jie-Ping Yu, Dan Li, Yue-Hong Huang, Zhi-Xin Chen, Xiao-Zhong Wang
Li-Juan Zhang, Jie-Ping Yu, Department of Gastroenterology, Renmin Hospital, Wuhan University Medical School, Wuhan 430060, Hubei Province, China
Dan Li, Yue-Hong Huang, 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 Science and Technology fund of Fujian Province, No. 2003D05
Correspondence to: Xiao-Zhong Wang, Department of Gastroenterology, Union Hospital of Fujian Medical University, Fuzhou 350001, Fujian Province, China.
Telephone: +86-591-3357896-8482
Received: June 16, 2003
Revised: July 20, 2003
Accepted: July 24, 2003
Published online: January 1, 2004

AIM: To observe the possible effects of transforming growth factor (TGF) β1, interleukin (IL)-6, tumor-necrosis factor (TNF) α and IL-10 on experimental rat hepatic fibrosis.

METHODS: One hundred SD rats were divided randomly into the three groups. Control group received intraperitoneal injection of saline (2 mL·kg-1), twice a week. Fibrogenesis group was injected intraperitoneally with 50% carbon tetrachloride (CCl4) (2 mL·kg-1) twice a week. Fibrosis-intervention group was given IL-10 at a dose of 4 μg·kg-1 20 minutes before CCl4 administration from the third week. At the fifth, seventh, and ninth weeks, 7 to 10 rats in each group were sacrificed to collect serum. Levels of TGF-β1, TNF-α, IL-6 and IL-10 were determined by enzyme-linked immunosorbent assay (ELISA). The liver tissues were taken for routine histological examination.

RESULTS: Hepatic fibrosis was developed with the injection of CCl4. Values of the circulating TGFβ1, TNFα, IL-6 and IL-10 in the control group were 25.49 ± 5.56 ng·L-1, 15.18 ± 3.83 ng·L-1, 63.64 ± 13.03 ng·L-1 and 132.90 ± 12.13 ng·L-1, respectively. Their levels in the CCl4-intoxication group were 31.13 ± 6.41 ng·L-1, 18.91 ± 5.31 ng·L-1, 89.08 ± 25.39 ng·L-1 and 57.63 ± 18.88 ng·L-1, respectively, and those in the IL-10-intervention group were 26.11 ± 5.32 ng·L-1,13.99 ± 1.86 ng·L-1, 74.71 ± 21.15 ng·L-1 and 88.19 ± 20.81 ng·L-1, respectively. A gradual increase was observed in the levels of TGFβ1, TNFα and IL-6 during hepatic fibrogenesis. These changes were partially reversed by simultaneous administration of IL-10. The histological parameters, characterized by CCl4-intoxification, also seemed to be improved with IL-10 treatment, the collagen production was reduced at the ninth week and the histological activity index was decreased from 7.9 ± 1.2 to 4.7 ± 0.9.

CONCLUSION: TGFβ1, TNFα and IL-6 may play important roles during CCl4-induced hepatic fibrogenesis, and IL-10 may counterbalance their effects.

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