| Rheumatoid arthritis (RA) is an autoimmune disease that expresses chronic inflammation in synovial tissues and joints and develops into impaired joint function. The prevalence of RA varies worldwide between 0.5% and 1%. Genetic, hormonal, and environmental factors contribute to its development. A major obstacle to the development of rational treatment strategies is that the disease mechanisms and the causative environmental and genetic factors remain largely unknown. Clues may come from experimental arthritis.Glucosides of chaenomeles speciosa (GCS) was from Chaenomeles speciosa [sweet] Nakai, is a Chinese traditional herbal medicine (CTM). Effective parts and chemical constituents of GCS were extracted and purified by methods of solvent extraction, column chromatography, layer chromatography, et al.Collagen-induced arthritis (CIA) is a well-known disease model for RA. CIA resembles RA in a number of pathological, histological, and immunological aspects. Features of CIA include chronic synovitis, inflammatory cell infiltration, pannus formation, destruction of cartilage, and bone erosion.. Immune mechanisms that include both humoral and cellular immunity to CII have been implicated in the pathogenesis of the disease. Furthermore, the similarities between the joint pathology in CIA and RA are most widely used for studies ofRA pathogenesis and for screening of new drugs for treatment of rheumatoid disease. This study delineates the disease course, the influenceof the organ-and tissue-specificity of inflammation, and the dynamics of the joint inflammation including infiltrating cell types, the influence of T cells, the humoral and cellular reactivity to the arthritogenic cartilage autoantigens rat collagen type II (CII). The goal of this study was to extend our understanding of the roles played by GCS in the pathogenesis of arthritic diseases by interfering with cytokine-signaling pathways.Our study also aimed to develop a new therapeutic strategy for the treatment of RA by blockade of intracellular cytokine-signaling pathways. To further confirm the actions of such anti-inflammation and immunoregulation, we investigated in this paper the effects and mechanisms of GCS on G protein-AC-cAMP transmembrane signal transduction at levels of organ, cell, molecule, expression of mRNA respectively. 1.Effects of GCS on inflammatory and immune responses of collagen-induced arthritis in vivoCIA model was induced by native chicken type II collagen that had been dissolvedovernight at 4C in 0.1 M acetic acid (4 mg mL-1) and emulsified with an equal volumeof Freund' s incomplete adjuvant (FIA). Hind paw volumes of rats were measured by volume meter ( A ml) and arthritis index was evaluated at the same time; weight gain and arthritis index of immune organ(thymus and spleen) were also examined; antibodies to CII was determined by ELISA and the delayed-type hypersensitivity( DTH) ( A mm) was also examined; The legs and hind paws of rats were removed, fixed with 10% paraformaldehyde in PBS, and then decalcified for 10 days with EDTA and embedded in paraffin for histologic analysis. The paraffin sections were stained with hematoxylin and eosin; It was shown that the administration of GCS(30,60,120mg.kg-1 ,igX 7d) inhibited the inflammatory response and restored body weight and the weight of immune organs _ of CIA rats. GCS had no effect on the concentration of antibodies to CII. It was foundthat there were increases of lymphocyte proliferation IL-2 production and synoviocytes proliferation in CIA rats, together with IL-1 and TNF- a in peritoneal macrophages. GCS reduced above changes significantly and had good effect on the progressiveinflammatory,degeneration of synovial, cartilage, and bone in arthritic joints of CIArats.2. Effects of GCS on immune cells and cytokines of collagen-induced arthritis invivo and in vitroConA and LPS-induced lymphocytes proliferation,the production of interleukin-2 (IL-2) secreted by thymus, the production of interleukin-1(IL-1) secreted by peritoneal macrophag...
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