Effects and mechanisms of glucosides of chaenomeles speciosa on collagen-induced arthritis in rats.
Effects of glucosides of chaenomeles speciosa (GCS)-a Chinese traditional herbal medicine (CTM) on inflammatory and immune responses and its mechanisms in collagen-induced arthritis (CIA) rat were studied. Hind paw volumes of rats were measured by volume meter; lymphocyte proliferation, interleukin-1, interleukin-2, TNF-alpha level was determined by 3-(4,5-2 dimethylthiazal-2yl)2,5-diphenyltetrazoliumbromide (MTT) assay; cAMP level in synoviocytes was analyzed by competitive protein binding assay (CPBA). mRNA expression of G(i,), G(s), and TNF-alpha of synoviocytes in CIA rats was measured by RT-PCR and antibodies to collagen type II (CII) were determined by enzyme-linked immunosorbent assay (ELISA), respectively. There was a marked secondary inflammatory response in CIA model, which accompanied with the decrease of body weight and the weight of immune organs simultaneously. The administration of GCS (30, 60, 120 mg x kg(-1), ig x 7 days) inhibited the inflammatory response and restored body weight and the weight of immune organs of CIA rats. Lymphocyte proliferation and IL-2 production of CIA rats increases, together with IL-1 and TNF-alpha in peritoneal macrophages and synoviocytes. The administration of GCS (30, 60, 120 mg x kg(-1), ig x 7 days) reduced above changes significantly. GCS at the concentration of 0.5, 2.5, 12.5, 62.5, 125 mg x l(-1) increased cAMP level of synoviocytes, which decreased in CIA rats in vitro. At the same time, GCS inhibited mRNA expression of G(i,) and TNF-alpha of synoviocytes and increased mRNA expression of G(s) of synoviocytes in CIA rats. GCS had no effect on the concentration of antibodies to CII. GCS possesses anti-inflammatory and immunoregulatory actions and has a therapeutic effect on CIA rats due to G protein-AC-cAMP transmembrane signal transduction of synoviocytes, which play a crucial role in pathogenesis of this disease.
Chen
Qun
Q
Institute of Clinical Pharmacology, Anhui Medical University, 230032 Hefei, China. chenq2001@163.net
Wei
Wei
W
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D001169:Arthritis, Experimental / Q000188:drug therapy* / Q000276:immunology; D002455:Cell Division / Q000187:drug effects / Q000276:immunology; D003094:Collagen; D024043:Collagen Type II / Q000276:immunology; D000242:Cyclic AMP / Q000096:biosynthesis / Q000276:immunology; D004365:Drugs, Chinese Herbal / Q000627:therapeutic use*; D004797:Enzyme-Linked Immunosorbent Assay; D005960:Glucosides / Q000627:therapeutic use*; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D007375:Interleukin-1 / Q000096:biosynthesis / Q000276:immunology; D007376:Interleukin-2 / Q000096:biosynthesis / Q000276:immunology; D017746:Joint Capsule / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D027824:Rosaceae / Q000737:chemistry*; D013154:Spleen / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D013950:Thymus Gland / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000276:immunology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D024043:Collagen Type II; D004365:Drugs, Chinese Herbal; D005960:Glucosides; D007375:Interleukin-1; D007376:Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D003094:Collagen; D000242:Cyclic AMP