Expression of IL-17 and TNF-α in Collagen-induced Arthritis Rats Model
Gao Jin-fang
Abstract
Gao Jin-fang
Abstract
Objective To detect the expression characteristics of IL-17 and TNF-α in collagen-induced arthritis(CIA) rats model.Methods To establish the collagen-induced arthritis rats model was established,then the serum level of IL-17 and TNF-α were determined by ELISA,and the degree of pathogenicity as well as the pathological characteristics were assayed by histopathological techniques and joint roentgenography.Results In CIA model the level of IL-17 and TNF-α measured by ELISA were significantly higher than those of the normal group(P 0.05).As demonstrated by histopathology and roentgenography,typical arthritis pathology with chronic proliferative synovitis and secondarily destroyed articular cartilage and bone was found.Conclusion The animal model with CIA was successfully established in this experi-ment.The serum level of IL-17 and TNF-α increased significantly,indicating that IL-17 might involved in the pathogenesis of rheumatoid arthritis.
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Objective To detect the expression characteristics of IL-17 and TNF-α in collagen-induced arthritis(CIA) rats model.Methods To establish the collagen-induced arthritis rats model was established,then the serum level of IL-17 and TNF-α were determined by ELISA,and the degree of pathogenicity as well as the pathological characteristics were assayed by histopathological techniques and joint roentgenography.Results In CIA model the level of IL-17 and TNF-α measured by ELISA were significantly higher than those of the normal group(P 0.05).As demonstrated by histopathology and roentgenography,typical arthritis pathology with chronic proliferative synovitis and secondarily destroyed articular cartilage and bone was found.Conclusion The animal model with CIA was successfully established in this experi-ment.The serum level of IL-17 and TNF-α increased significantly,indicating that IL-17 might involved in the pathogenesis of rheumatoid arthritis.
Key concepts: Arthritis, Histopathology, Rheumatoid arthritis, Synovitis, Pathogenesis, Medicine, Pathological, Tumor necrosis factor alpha