4.4 Article

Protective effects of quercetin against inflammation and oxidative stress in a rabbit model of knee osteoarthritis

Journal

DRUG DEVELOPMENT RESEARCH
Volume 80, Issue 3, Pages 360-367

Publisher

WILEY
DOI: 10.1002/ddr.21510

Keywords

inhibitor of metalloproteinases-1; matrix metalloproteinase-13; osteoarthritis; quercetin

Funding

  1. Science and Technology Project of Yongkang City, Zhejiang Province [201721]

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This study investigated the effects of a natural phenolic compound quercetin on surgical-induced osteoarthritis (OA) in rabbits. Forty-eight New Zealand White rabbits were used to establish OA model by Hulth modified method, and subsequently randomized into untreated OA group (treatment was drinking water), celecoxib treated group (celecoxib 100 mg kg-1 by gavage), and quercetin treated group (25 mg kg-1 by gavage). Sixteen nonoperated rabbits served as the normal controls (drinking water was given). The treatment (length: 4 weeks) started on the 5th week postoperation when the OA pathological changes were manifested. Expressions of superoxide dismutase (SOD), matrix metalloproteinase-13 (MMP-13) and tissue inhibitor of metalloproteinases-1 (TIMP-1) in serum, synovial fluid, and synovial tissue were measured at 8 and 12 weeks postoperation. Pathological analysis was performed with synovial tissue section and Osteoarthritis Research Society International histopathology grading and staging scores were determined. The quercetin treated group showed higher SOD and TIMP-1 expressions but lower MMP-13 expression than untreated OA group in the serum, synovial fluid and synovial tissues (p <.05). There was no significant difference in the SOD, MMP-13 and TIMP-1 expressions between the quercetin-treated and celecoxibtreated groups. The MMP-13/ TIMP-1 ratio of the quercetin treated group was significantly lower than that of the untreated OA group (p <.05). Quercetin can up-regulate SOD and TIMP-1, downregulate MMP-13, and improve the degeneration of OA through weakening the oxidative stress responses and inhibiting the degradation of cartilage extracellular matrix.

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