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DMN과 GALN에 의한 간세포손상이 신사구체의 면역글로부린 침착에 미치는 영향에 관한 실험적 연구
전호종,설주문,김수홍 朝鮮大學校 附設 醫學硏究所 1992 The Medical Journal of Chosun University Vol.17 No.2
Glomerular IgA deposition often occured in prolonged hepatobiliary disease and also it's definite pathogenesis is not yet cleared, In the present study, liver injury was induced by intraperitoneal administration of single dose of dimethylnitrosamine and D-galactosamine in rats to investigate the pathogenesis of glomerular Ig A deposition by observations of immunohistochemical and special stains. The results obtained were as follows 1. In the dimethylnitrosamine-treated rats, there were extensive blood-filled necrotic spaces containing debris of necrotic hepatocytes and sinusoidal lining cells in the centrilobular areas 5 days after intraperitoneal administration. 2. In the D-galactosamine treated rats, spotty necrosis with inflammatory cell infiltration throughout the lobule, and swelling and increment of Kupffer cells were appeared 2 days after intraperitoneal administration. 3. There were slightly increased thickness of renal glomerular basement membrane and widening of the mesangeal matrix in dimethylnitrosamine-treated rats, 14 days after intraperitoneal administration, but no pathological changes were observed in glomerular basement membrane and mesangeal cells in D-galactosamine treated rats. 4. There were glomerular IgA deposition after a single dose administration of dimethylnitrosamine. Slight deposits of IgA appeared 2 days after administration, In 5 days after administration, the deposits gradually intensified and peaked at 14 days after administration, However in the D-galactosamine-treated rats, only slight deposits of IgA appeared at days 7 and 14 There were no depositions of IgG in the dimethylnitrosamine and D-galactosamine treated rats. 5. These results suggest that dysfunction of the hepatocytes and Kupffer cells contribute to glomerular IgA deposition.
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肝炎에서 增殖된 α-smooth muscle actin의 表現 樣相
기근홍,조국형,설주문 朝鮮大學校 附設 醫學硏究所 1992 The Medical Journal of Chosun University Vol.17 No.2
α-smooth muscle actin is an actin isoform typical of smooth muscle cells, and could be a reliable marker for phenotypic modulation toword smooth muscle cells. Six major isoforms of actin have been discribed. The materials for our study consisted of 50 chronic active hepatitis (10 mild, 15 moderate, 15 severe, and 10 precirrhotic change) and 25 chronic persisitent hepatitis, that biopsied for diagnosis at Chosun University Hospital from January, 1989 to May, 1992. All cases were performed of hematoxylin-eosin stain, PAS stain, Masson-trichrome stain, reticulin stain, and immunohistochemical stain of α-smooth muscle actin, vimentin and desmin by ABC method using micro-probe system. Immunoreactivity was evaluated and compared with the reactivity of a-smooth muscle actin, vimentin and desmin. The results obtained were as follows 1. In the chronic persistent hepatitis, α-smooth muscle actin positive cells appeared in the vascular smooth muscle cells of perisinusoidal spaces and limiting plate area. 2. With the progression of grade in chronic active hepatitis, α-smooth muscle actin positive cells were recognized in the perisinusoidal spaces, fibrotic area, and area of regenerating nodule. In conclusion, α-smooth muscle actin is a good marker for the detection of fibroblasts, myofibroblasts and myofibroblast-like cells. So α-smooth muscle actin was helpful diagnostic aid in differentiation of chronic active hepatitis and chronic persistent hepatitis.
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