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The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
Published on: June 17, 2016
Immunohistochemical study of macrophage migration inhibitory factor in rat liver fibrosis induced by thioacetamide
1Department of Food and Nutrition, Hakodate Junior College, Hakodate, Japan.
Abstract:
Macrophage migration inhibitory factor (MIF) is a molecule known to regulate macrophage accumulation at sites of inflammation. To elucidate the role of MIF in progression of liver fibrosis, the immunohistochemical localization of MIF and macrophages in the liver were examined. Male Wistar rats received thioacetamide (TA) injections (200 mg/kg, i.p.) for 1 or 6 weeks. In biochemical and histological tests, it was confirmed that liver fibrosis was induced. In immunohistochemical analyses, the expression of MIF protein was seen in hepatocytes in the areas extending out from the central veins to the portal tracts. In particular, at 6 weeks, immunoreactivity was detected in degenerated hepatocytes adjacent to the fibrotic areas but hardly observed in the fibrotic areas. On the other hand, a number of exudate macrophages stained by antibody ED1 were seen in the areas from the central veins to the portal tracts at 1 week and in the fibrotic areas at 6 weeks. Macrophages also showed a significant increase in number as compared with controls. These results revealed that there was a close relationship between the appearance of MIF expression and ED1-positive exudate macrophages in degenerated hepatocytes during the progression of TA-induced liver fibrosis.
Insights
Macrophage migration inhibitory factor (MIF) expression correlates with macrophage accumulation in degenerated hepatocytes during liver fibrosis progression. This study examines MIF and macrophage roles in thioacetamide-induced liver fibrosis in rats.
Area of Science:
- Hepatology
- Immunology
- Pathology
Background:
- Macrophage migration inhibitory factor (MIF) regulates macrophage accumulation in inflammatory sites.
- The role of MIF in liver fibrosis progression remains incompletely understood.
Purpose of the Study:
- To investigate the role of MIF in the progression of liver fibrosis.
- To examine the immunohistochemical localization of MIF and macrophages in thioacetamide-induced liver fibrosis.
Main Methods:
- Male Wistar rats were injected with thioacetamide (TA) for 1 or 6 weeks to induce liver fibrosis.
- Immunohistochemical analyses were performed to detect MIF protein and ED1-positive macrophages.
- Biochemical and histological tests confirmed liver fibrosis induction.
Main Results:
- MIF protein expression was observed in hepatocytes, particularly in degenerated hepatocytes near fibrotic areas at 6 weeks.
- A significant increase in ED1-positive exudate macrophages was noted in affected liver areas.
- A close relationship was found between MIF expression and macrophage appearance in degenerated hepatocytes during fibrosis progression.
Conclusions:
- MIF expression in degenerated hepatocytes is closely associated with macrophage infiltration during liver fibrosis.
- These findings suggest a potential role for MIF-macrophage interactions in the pathogenesis of liver fibrosis.
