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The Effect of Immune Tolerance Induced by β2 Adrenalin Receptor Signal Transduction on Mesenteric Lymph Node Lymphocytes in Rats with Collagen-induced Arthritis and the Effect of Chicken Type II Collagen

Author: ZhaoWei
Tutor: MaYong;WeiWei
School: Anhui Medical University,
Course: Pharmacology
Keywords: collagen-induced arthritis chicken typeⅡcollagen β2-adrenergic receptor mesenteric lymph node lymphocytes immune tolerance desensitization
CLC: R684.3
Type: Master's thesis
Year: 2011
Downloads: 35
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Abstract


OBJECTIVE According to the changes of paw swelling, histological morphological of mesenteric lymph nodes (MLNs) and synovium of collagen-induced arthritis (CIA) rats, to study the effect of CCⅡon the CIA rats. we designed the beta2-adrenergic receptor (β2-AR) of MLNLs to investeigate the mechanisms of MLNLs proliferation and the effects of CCⅡon the expression ofβ2-AR, GRK2, GRK3, Gαs andβ-arrestin1, 2 and the desensitization of MLNLs in CIA rats and the effects of G protein-AC-cAMP transmembrane signal transduction on the proliferation of MLNLs in CIA rats.METHODS The model of CIA rats were induced by injection of CCⅡemulsion. CCⅡ(10, 20, 40μg·kg-1·d-1, ig, d14-d21) was administrated intragastricly to CIA rats. Secondary paw swelling of CIA rats was measured by volume meter. Histopathological change of MLNs and synovium were observed by light microscope. The expression ofβ2-AR, GRK2, GRK3 andβ-arrestin1, 2 was measured by western blot and immunohistochemistry analysis, respectively. Fractionating Membrane and Cytoplasm,β2-AR, GRK2, Gαs and beta-arrestin1, 2 distribution was measured by western blot in cytoplasm and membrane fractions. The expression change of cAMP was investigated by radioimmunoassay.RESULTS(1)CCⅡrelieves joints swelling、changes inflammation of MLNs and synovium in CIA ratsInflammatory reaction occurred on d26 after immunization. There was a marked secondary inflammatory response in the models, which accompanied with paw swelling, pain, polyarthritis, decrease of body weight, and the development of inflammatory lesions. Compared with the normal rats, in CIA rats, the histological morphological examination of rats knee joints showed hyperplastic synovium, synovial lining hyperplasia, inflammatory cells infiltration. The MLNs of CIA represented that lymphatic follicle was hyperplastic and the number of inflammatory cells. It was found that CCⅡ(10, 20, 40μg·kg-1·d-1, ig, d14-d21) significantly suppressed secondary hind paw swelling and polyarthritis index, as well as improved arthritic status histological of MLNs and synovium in CIA rats.(2)CCⅡdecreasing the proliferation of MLNLs and up-regulating the level of cAMP CCⅡ(10, 20, 40μg·kg-1·d-1, ig, d14-d21)inhibited the highered proliferation of MLNLs, and up-regulated the level of cAMP of MLNLs in CIA rats. The results suggested that one of characteristic effects of CCⅡon exerting therapy rats CIA is inhibiting the proliferation of MLNLs and up-regulating the level of cAMP.(3)Enhancing desensitization, and recovering the balance of the expression of GRK2/β-arrestin1, 2 proteins and recovering G protein-AC-cAMP signal transduction of MLNLs in CIA rats was one of the most important mechanisms of up-regulating the level of cAMP, inhibiting the proliferation of the lymphocytesCCⅡ(10, 20, 40μg·kg-1·d-1, ig, d14-d21) increased total protein expressions ofβ2-AR, GRK2 and GRK3 and decreased that ofβ-arrestin1, 2 of MLNLs in CIA rats. CCⅡfurther increased plasmatic protein expressions of GRK2, Gαs and decreased that ofβ-arrestin1, 2,β2-AR and increased membrane protein expressions ofβ2-AR, GRK2, Gαs and decreased that ofβ-arrestin1, 2 of MLNLs in CIA rats. The results suggested that CCⅡEnhancedβ2-AR desensitization, recovered the balance of the expression of GRK2/β-arrestin1, 2 proteins and recovered G protein-AC-cAMP signal transduction and induced immune tolerance of MLNLs in CIA rats.CONCLUSIONS(1)CCⅡsuppressed secondary hind paw swelling and improved arthritic status histological of mesenteric lymph node in CIA rats. CCⅡinhibited the highered proliferation of MLNLs, and up-regulated the level of cAMP of MLNLs in CIA rats. The result suggested that CCⅡmight regulate the G protein-AC-cAMP transmembrane signal transduction to regulate the level of cAMP and to inhibit the proliferation of MLNLs in CIA rats.(2)CCⅡsignificantly increased the expression levels ofβ2-AR and GRK2 protein, decreased the elevated expression level ofβ-arrestin1, 2 protein, enhancedβ2-AR desensitization, and regulated the balance of GRK2/β-arrestin1, 2 in MLNLs in CIA rats. Enhancingβ2-AR desensitization, and regulating the balance of expression of GRK2/β-arrestin1, 2 proteins from MLNLs in CIA rats is one of the most important mechanisms of CCⅡup-regulating the level of the cAMP and inhibiting proliferation of the lymphocytes.

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CLC: > Medicine, health > Surgery > Orthopaedic Surgery ( movement system diseases,orthopedic surgery ) > Joint disease and injury > Arthritis
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