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- Sequential Studies of Glomerular Crescent Formation in Rabbits with Anti-Glomerular Basement Membrane(GBM) Antibody Induced Glomerulonephritis(GN).
- Hye Seon Ahn, Jung Woo Noh, Moon Hyang Park
- Korean J Pathol. 1997;31(3):219-232.
- 1,629 View
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Abstract
PDF - To investigate the mechanism of crescent formation, sequential pathologic changes from the New Zealand White rabbits with anti-GBM antibody induced GN by administration of guinea pig anti-GBM IgG were studied by light (LM), immunofluorescent (IF) and electron (EM) microscopy. Although no glomerular changes were observed in LM, swelling of the endothelial cells and the epithelial cells were noted in EM by day 2. By day 7, early and cellular crescents were evident. Proteinaceous materials and fibrins were noted in the glomerular capillary lumina (GCL) and Bowman's space (BS) associated with segmental hypercellularity. The GBM damage became progressively severe, followed by focal detachment of the visceral epithelial cells from the GBM. At day 14, fibrin strands, mononuclear cells and collagen fibrils were present between the proliferating extracapillary cells. At day 31, fibrocellular crescents were predominated. Elongated spindle cells, morphologically resembling myofibroblasts, were noted near the Bowman's capsule (BC). A degree of tubular atrophy, interstitial fibrosis, and inflammatory infiltrates increased as it did with fibrous organization of crescent. Intense linear IF staining for IgG and C3 were seen throughout the experiments along the GBM. In conclusion, the progression of crescent from an early "proteinaceous" stage through cellular, fibrocellular and fibrous stages was well documented in this study. Inflammatory cells and coagulation mechanism may activate the initiation of the GBM damage at the early stage. Activated periglomerular mononuclear cells may also cause disruption of BC which facilitates entry of activated periglomerular cells and fibroblasts into BS leading to progressive fibrous crescent formation.
- Effect of Eicosapentaenioc acid and Butyrated hydroxyanisole on Hypercholestrolemic Diet Induced Atherogenesis in Rabbit.
- Choong Sik Lee, Jeung Mok Choi, Sung Ki Min, Kyu Sang Song, Dae Young Kang, Kyu Lym
- Korean J Pathol. 1994;28(3):235-245.
- 1,725 View
- 10 Download
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Abstract
- It has been suggested that the fish oil can reduce atherogenesis in humans and animals, and that peroxidation of lipoproteins may be a major factor causing atherosclerotic lesions. We tested these posibilities in rabbits fed an atherogenic diet by comparing the effect of a eicosapentaenoic acid(EPA: a major component of fish oil)supplement and a butyrated hydroxyanisole(BHA: antioxidant)diet supplement. Tweenty-eight young male New Zealand White rabbits were used in this study. The animals were divided by control, cholesterol fed only, cholesterol + EPA, and cholesterol + BHA groups. The experimental course lasted 12 weeks and animals were sacrificed periodically(2, 5, 8, 12weeks)for quantitative studies of aortic atherosclerosis using light and electron microscopy. Plasma cholesterol levels were determined and lipopreteins were separated periodically. The cholesterol fed only group showed an increased serum cholseterol level and atherosclerotic lesions from 5 weeks of experiments. The EPA supplement resulted in similiar serum cholesterol levels with cholesterol fed only group, but greater lesion than cholesterol fed only group. The BHA supplement resulted in higher serum cholesterol levels except VLDL-cholesterol than EPA supplement group. However, the atherosclerotic lesion was not increased. Our studies support the theory that oxidative modification of lipoproteins is important for the atherogenesis and antioxidant may have a protective effect. However, it failed to show antiatherogenesis effect of fish oil.
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