4.5 Article

Anti-inflammatory effect of resveratrol on adjuvant arthritis rats with abnormal immunological function via the reduction of cyclooxygenase-2 and prostaglandin E2

期刊

MOLECULAR MEDICINE REPORTS
卷 9, 期 6, 页码 2592-2598

出版社

SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2014.2070

关键词

adjuvant arthritis; resveratrol; immune; inflammation; rat

资金

  1. National Natural Science Foundation of China [81373421]
  2. Innovative Entrepreneurial Training of the National College Students' Program [201310366007]
  3. Natural Science Foundation of Higher Education Institutions of Anhui Province, China [KJ2010A183]

向作者/读者索取更多资源

Rheumatoid arthritis (RA) is a chronic inflammatory disease with unknown etiology. The present study investigated the anti-inflammatory effect of resveratrol on rats with adjuvant arthritis (AA) with abnormal immunological function via the reduction of cyclooxygenase-2 (COX-2) and prostaglandin E-2 (PGE(2)). AA model rats were established by injection of complete Freund's adjuvant and alterations in the rats secondary paw swelling and the polyarthritic scores were observed. Pathological examination of joint tissues was observed by hematoxylin and eosin staining. The proliferation of spleen cells was examined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay in vitro. The protein expression of COX-2 in the synovial tissues was detected by western blotting. The level of PGE2 in the serum was assayed using an ELISA kit. The results demonstrated that resveratrol (10 or 50 mg/kg) was able to significantly reduce paw swelling and decrease the arthritis scores. Compared with the AA model rats, a significant reduction in the proliferation of concanavalin A-stimulated spleen cells was observed, articular cartilage degeneration with synovial hyperplasia and inflammatory cell infiltration was suppressed and the production of COX-2 and PGE(2) in AA rats was reduced by treatment with resveratrol. These results suggest that resveratrol has significant anti-inflammatory effects on AA rats, which may be associated with the reduction of COX-2 and PGE(2) inflammatory mediators.

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