Effects of mast cells on degradation of collagen fibers in dimethylnitrosamine-induced hepatic fibrosis of rat.
- Author:
Yu-lan JIN
1
;
Quan ZHOU
;
Cheng TIAN
;
Hong-gang LIU
;
Yosihiro HAYASHI
;
Hideaki ENZAN
Author Information
- Publication Type:Journal Article
- MeSH: Actins; metabolism; Animals; Cell Count; Dimethylnitrosamine; Liver Cirrhosis; chemically induced; metabolism; pathology; Male; Mast Cells; metabolism; pathology; ultrastructure; Matrix Metalloproteinase 2; metabolism; Rats; Rats, Wistar; Tissue Inhibitor of Metalloproteinase-2; metabolism; Tryptases; metabolism
- From: Chinese Journal of Pathology 2012;41(4):260-264
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the relationship between mast cell and hepatic fibrosis by histopathological method and semi-quantitative measurement.
METHODSSeventy-two Wistary male rats, the control group and the normal group of each only 16, experimental group of 40 rat liver fibrosis was induced by injection of DMN and was sampled at eight different time points. HE, histochemistry, immunohistochemistry (ABC method) and immunofluorescence were performed. The size of fibrosis and the number of mast cells were counted. The expression of MMP-2 and TIMP-2 was documented and electron microscopic examination was performed.
RESULTSAfter injection of DMN, the fibrosis was the most severe in the 2 week (3.72%) and the first month (3.73%, P = 0.2626), and then gradually diminished, although residual fibrosis was still present at 12 months (1.42%, P = 0.0003). The appearance of mast cells began at 2 weeks (1.73 per 200 power field in average by light microscope) after the injection and reached the peak at 4 months (3.06, P = 0.008). Residual amount of mast cells were present at 12 months (1.04, P = 0.045). However, the degree of fibrosis was not proportional or overlapping with the number of mast cells in this experiment model. Mast cells expressed MMP-2 but not TIMP-2.
CONCLUSIONSIn the DMN-induced rat liver fibrosis model, mast cell may be an integral player in the pathogenesis of liver fibrosis and may contribute to the degradation of fibrosis by synthesizing and secreting MMP-2.