Original Articles
Copyright ©The Author(s) 1998. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 15, 1998; 4(3): 206-209
Published online Jun 15, 1998. doi: 10.3748/wjg.v4.i3.206
Study of heteroserum-induced rat liver fibrosis model and its mechanism
Zhi-Gang Huang, Wei-Rong Zhai, Yue-E Zhang, Xiu-Rong Zhang
Zhi-Gang Huang, Wei-Rong Zhai, Yue-E Zhang, Xiu-Rong Zhang, Department of Pathology, School of Basic Medical Sciences, Shanghai Medical University, Shanghai 200032, China
Zhi-Gang Huang, male, born on 1968-05-09 in Xiangfan City, Hubei Province, graduated from Shanghai Medical University as a postgraduate in 1996, now an attending physician of gastroenterology, working in the Department of Internal Medicine, Baoshan Central Hospital, Shanghai 201900, China, having 2 papers published.
Author contributions: All authors contributed equally to the work.
Correspondence to: Professor Wei-Rong Zhai, Department of Pathology, School of Basic Medical Sciences, Shanghai Medical University, Shanghai 200032, China
Telephone: +86-21-56601100-294
Received: February 18, 1998
Revised: April 20, 1998
Accepted: May 24, 1998
Published online: June 15, 1998
Abstract

AIM: To investigate the morphological changes in the process of heteroserum induced rat liver fibrosis and the mechanism of fibrogenesis of this model.

METHODS: A model of heteroserum-induced rat liver fibrosis was established by intraperitoneal injection of porcine serum. In addition to the observation of the morphological changes of this model, the infiltration of eosinophils and mast cells were measured quantitatively and the deposition of IgG and complement C3 was detected by immunofluorescence.

RESULTS: The rat liver fibrosis was induced successfully at the end of the 8th week after the injection of heteroserum. Besides the increase of hepatic stellate cells (HSC) during the process of liver fibrosis, proliferation and activation of primary mesenchyma cells (PMCs) were also found. In the early stage, the infiltration of eosinophils and mast cells was significantly increased and the deposition of IgG and complement C3 was positive in the portal tracts and septa, while gradually reduced after the injection was stopped.

CONCLUSIONS: This model is suitable for the research on liver fibrogenesis; the pathogenesis of this model may be related with the allergen-induced late phasereaction (LPR) caused by the injection of heteroserum, and the HSCs and the PMCs are important sources of ECM-producing cells.

Keywords: liver cirrhosis; heteroserum; disease models, animal; liver/pathology; mast cell; IgG; complement C3; rats