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Original Articles
- Cellular Distribution of TGF-beta1 Peptide in Dimethylnitrosamine Induced Fibrosis of Rat Liver.
- Sook Nyo Lee, Do Youn Park, Sun Kyung Lee
- Korean J Pathol. 1997;31(11):1157-1165.
- 1,562 View
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Abstract
- Recently attention has been focused on the biology of transforming growth factor-beta1 (TGF-beta1). TGF-beta1, a potent regulator of cell proliferation, stimulates the proliferation of many cell types of mesenchymal origin and inhibits the growth of many epithelial cells. But its cellular distribution and temporal expression remain unknown. The aim of this study was to investigate immunohistochemically the cellular distribution and temporal expression of TGF-beta1 during rat hepatic fibrosis induced by dimethylnitrosamine (DMN). At an early stage of liver fibrosis, there was evidence of multiple centrilobular hemorrhagic necrosis with parenchymal lobular collapse, and at a late stage, there was septal fibrosis with micronodule formation of the parenchyme. TGF-beta1 peptide was first expressed in centrilobular clusters of macrophage which were surrounded by many TGF-beta1 negative fat-storing cells (FSCs). Along with the progression of fibrosis, the TGF-beta1 peptide was expressed in the alpha-smooth muscle actin positive FSCs and also in some peripherally located hepatocytes of micronodules. Serum IFN-gamma was detected in the serum 2 weeks after an initial administration of DMN had reached the peak level at the 4th week and then markedly decreased at the 5th week. We think that TGF-beta1 peptide is produced by macrophages influenced by soluble IFN-gamma, and is expressed in the -smooth muscle actin positive mesenchymal cells and regenerating hepatocytes, and that this cytokine may have an important role in the synthesis of the extracellular matrix and in the regulation of hepatocytic regeneration.
- A Pathological Study of Phenol Induced Hepatic and Gastrointestinal Lesions.
- Dae Young Kang
- Korean J Pathol. 1993;27(6):561-572.
- 1,477 View
- 16 Download
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Abstract
PDF - In an attempt to elucidate the pathological effects of phenol, the present study was undertaken in male Sprague-Dawley rats. The control group of animals was fed a basal diet, and potable underground water. The experimental group of animals was fed a basal diet and potable underground water containing 30ppm, 60ppm, and 1% phenol with once a week administration of dimethylnitrosamine(DMN) 10 mg/kg I.P. Each group of animals was sacrificed on the 3rd, 6th, and 9th month. The liver and gastrointestinal tract were examined light microscopically, along with transmission electron microscopic studies of the liver and scanning electron microscopic studies of the gastric mucosa. The results were as follows: 1) In the acute phenol intoxicated group, the liver showed fatty changes in the hepatocytes with mitochondrial membrane destruction and myelin figure formation. 2) In the chronic phenol intoxicated group, fatty changes in the liver were observed. In addition, there was chronic inflammation in the gastrointestinal tract, with gastric mucosal erosion and central necrosis of the hepatic lobules, especially in the high phenol contaminated water treated group. 3) As a result of the examination under the light microscope, the DMN treated group showed hyperplastic nodules and liver cell dysplasia, the degree of which was proportional to the duration of the experiment, and was more severe in the DMN + phenol treated group. 4) As a result of the examination under the electron microscope, fatty changes in the liver, pleomorphism of the mitochondria and loss or shortness of bile canalicular microvilli in the DMN + phenol treated group were more severe than in the group treated only with DMN. In summary, the results obtained by the present study indicate chronic highly concentrated phenol intoxication induce liver cell necrosis and chronic inflammatory with a hepatotoxin such as DMN.
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