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Abstract
The pathogenesis of septal hepatic fibrosis, induced in rats by Capillaria hepatica infection, was studied with the aid of a large collection of stored paraffin blocks, representative of the different evolutive phases of fibrosis which appeared in 100% of infected rats. Studies were conducted involving histology, immunohistochemistry, immunofluorescence and morphometric methods, in order to observe the dynamic behavior of the cellular and matrix components of fibrosis, over a one year period of evolution. Observation verified that septal fibrosis originates from several portal spaces simultaneously. Its origin and progression involve blood vessel proliferation (angiogenesis), multiplication of actin-positive cells (pericytes and myofibroblasts) and progressive collagen deposition. By the end of 4-5 months, a progressive decrease in all these components was observed, when signs of regression of septal fibrosis became more evident over time. Besides indicating the fundamental role played by angiogenesis in the pathogenesis of fibrosis, these morphological data concerning the dynamics of this C. hepatica experimental model proved to be adequate for future investigations regarding the functional aspects of fibrosis induction, progression and regression.
Highlights
INTRODUCTIONHepatic fibrosis is a common complication for many types of hepatic diseases, especially those that are inflammatory, but its pathogenesis still presents complex features that keep stimulating research[1,2]
Recent data from our laboratory have indicated a dual and paradoxical role for angiogenesis, since it is ostensibly present during fibrosis formation[7], and during fibrosis regression[8]. These dynamic aspects of fibrogenesis appeared suitable for investigation with the aid of a peculiar experimental model of hepatic fibrosis, one which appears in 100% of rats infected with nematode worm Capillaria hepatica
The peculiarities of this experimental model of liver fibrosis may be explored for the study of several features of hepatic fibrosis biology, especially those related to dynamic changes in the cellular and matrix that occur at fibrosis initiation, progression, and regression
Summary
Hepatic fibrosis is a common complication for many types of hepatic diseases, especially those that are inflammatory, but its pathogenesis still presents complex features that keep stimulating research[1,2]. Recent data from our laboratory have indicated a dual and paradoxical role for angiogenesis, since it is ostensibly present during fibrosis formation[7], and during fibrosis regression[8] These dynamic aspects of fibrogenesis appeared suitable for investigation with the aid of a peculiar experimental model of hepatic fibrosis, one which appears in 100% of rats infected with nematode worm Capillaria hepatica. Rats infected with the nematode C. hepatica invariably develop a peculiar process of diffuse septal fibrosis of the liver that starts within 14-18 days following infection, becomes progressively intensified during the following 2-3 months and gradually decreases thereafter, remaining as a few, scattered, thin vascular fibrous septa, from six months up to at least a year. Particular attention was paid to the behavior of these elements during the periods of induction, progression and regression of septal fibrosis of the liver
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