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Journal Article
Research Support, Non-U.S. Gov't
Glucosides of Chaenomeles speciosa remit rat adjuvant arthritis by inhibiting synoviocyte activities.
Acta Pharmacologica Sinica 2003 November
AIM: To investigate the effects of Glucosides of Chaenomeles speciosa (GCS) on rat adjuvant arthritis (AA) and to clarify the role of synoviocytes in this process.
METHODS: Complete Freund's adjuvant was used to induce AA in rats. Secondary paw swelling of AA rats was measured with MK-550 volume meter. The pain response and polyarthritis index were scored. Synoviocytes were separated by incubation of collagenase and trypsin, and morphological changes of synoviocytes were observed by transmission electron microscope. Interleukin-1 (IL-1) production was measured by thymocyte proliferation assay. Tumor necrosis factor (TNFalpha) and prostaglandin E2 (PGE2) production were determined by radioimmunoassay.
RESULTS: There were significant secondary inflammatory reactions in AA rats. The morphology of synoviocytes from AA rats was changed, companying the elevation of the level of IL-1,TNFalpha, and PGE2 produced by synoviocytes from AA rats. GCS (60 and 120 mg/kg, ig, 8 d) suppressed secondary inflammatory paw swelling, pain response, and polyarthritis index. It also improved ultrastructural changes of synoviocytes and inhibited IL-1,TNFalpha, and PGE2 production in AA rats. The inhibitory effect of GCS 120 mg/kg was more evident than that of Actarit 60 mg/kg.
CONCLUSION: GCS reduced the secondary inflammatory in AA rats, which is associated with prevention of ultrastructural changes of synoviocytes and inhibition of secretion of proimflammatory cytokines.
METHODS: Complete Freund's adjuvant was used to induce AA in rats. Secondary paw swelling of AA rats was measured with MK-550 volume meter. The pain response and polyarthritis index were scored. Synoviocytes were separated by incubation of collagenase and trypsin, and morphological changes of synoviocytes were observed by transmission electron microscope. Interleukin-1 (IL-1) production was measured by thymocyte proliferation assay. Tumor necrosis factor (TNFalpha) and prostaglandin E2 (PGE2) production were determined by radioimmunoassay.
RESULTS: There were significant secondary inflammatory reactions in AA rats. The morphology of synoviocytes from AA rats was changed, companying the elevation of the level of IL-1,TNFalpha, and PGE2 produced by synoviocytes from AA rats. GCS (60 and 120 mg/kg, ig, 8 d) suppressed secondary inflammatory paw swelling, pain response, and polyarthritis index. It also improved ultrastructural changes of synoviocytes and inhibited IL-1,TNFalpha, and PGE2 production in AA rats. The inhibitory effect of GCS 120 mg/kg was more evident than that of Actarit 60 mg/kg.
CONCLUSION: GCS reduced the secondary inflammatory in AA rats, which is associated with prevention of ultrastructural changes of synoviocytes and inhibition of secretion of proimflammatory cytokines.
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