Vicenin 3 ameliorates ECM degradation by regulating the MAPK pathway in SW1353 chondrocytes

Aberrant destruction of the articular extracellular matrix (ECM) has been considered to be one of the pathological features of osteoarthritis (OA) which results in chondrocyte changes and articular cartilage degeneration. The MAPK signaling pathway serves a key role by releasing cartilage-degrading enzymes from OA chondrocytes. However, the use of MAPK inhibitors for OA is hindered by their potential long-term toxicity. Vicenin 3 is one of the major components of the Jian-Gu injection which is effective in the clinical treatment of OA. However, its potential impact on OA remain poorly understood. Therefore, the present study aimed to assess the effects of vicenin 3 on interleukin (IL)-1 beta-treated SW1353 chondrocytes, which mimic the microenvironment of OA. These chondrocytes were pretreated with vicenin 3 (0, 5 and 20 mu M) for 1 h and subsequently stimulated with IL-1 beta (10 ng/ml) for 24 h. Nitric oxide (NO) production was measured using the Griess reaction, whereas the production of prostaglandin E2 (PGE2), matrix metalloproteinases (MMPs), A disintegrin-like and metalloproteinase with thrombospondin motifs (ADAMTSs), collagen type II and aggrecan were measured using ELISA. The mRNA expression of MMPs and ADAMTSs were measured using reverse transcription-quantitative PCR. The protein expression levels of MAPK were measured using western blotting. Vicenin 3 was found to significantly inhibit IL-1 beta-induced production of NO and PGE. Increments in the expression levels of MMP-1, MMP-3, MMP-13, ADAMTS-4 and ADAMTS-5 induced by IL-1 beta, in addition to the IL-1 beta-induced degradation of collagen type II and aggrecan, were all reversed by vicenin 3 treatment. Furthermore, vicenin 3 suppressed IL-1 beta-stimulated MAPK activation, an effect that was similar to that exerted by SB203580, a well-known p38 MAPK inhibitor. In conclusion, vicenin 3 may confer therapeutic potential similar to that of the p38 MAPK inhibitor for the treatment of OA.