Effects and mechanisms of catechin for adjuvant arthritis in rats |
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Authors: | Li-Qin Tang Wei Wei Xiao-Yu Wang |
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Affiliation: | (1) Institute of Clinical Pharmacology Key Laboratory of Anti-inflammatory and Immune Pharmacology Department of Pharmacy/Affiliated Anhui Provincial Hospital, Anhui Medical University, China;(2) Institute of Clinical Pharmacology Key Laboratory of Anti-inflammatory and Immune Pharmacology, Anhui Medical University Anhui Province, 230032 Hefei, PR China |
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Abstract: | The present study was carried out to investigate the effects of catechin on adjuvant arthritis (AA) in the rat and its possible mechanisms of action. AA was induced by metatarsal footpad injection with complete Freund’s adjuvant in male Sprague-Dawley rats. The secondary inflammatory reaction was evaluated through assessment of hind paw swelling, polyarthritis index, and pain response. Proliferation of synoviocytes and the activity of interleukin-1 were examined by 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Tumor necrosis factor-α, prostaglandin E2 (PGE2), and cyclic adenosine monophosphate levels in synoviocytes were measured by radioimmunoassay. The PGE2 receptor, EP2, was analyzed by Western blot analysis. Intragastric administration of catechin (60 and 120 mg/kg) significantly suppressed secondary inflammatory paw swelling, pain response, and polyarthritis index. It also inhibited production of interleukin-1, tumor necrosis factor-α, and PGE2 and increased cyclic adenosine monophosphate levels in rats with AA. In the immunoblot analysis, catechin could upregulate expression of EP2 in the synoviocytes of rats with AA. The results showed that catechin reduced secondary inflammation in rats with AA; this outcome reflects its ability to mediate cAMP levels, upregulate expression of EP2, and inhibit secretion of proinflammatory cytokines in rats with AA. |
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Keywords: | catechin adjuvant arthritis (AA) cytokines cAMP EP2 |
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