| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1928355 | Biochemical and Biophysical Research Communications | 2014 | 5 Pages |
•DMF inhibits the expression of MMP-1, MMP-3, and MMP-13.•DMF ameliorated collagen type II degradation induced by TNF-α.•DMF suppresses JAK/STAT3 pathway.
Degradation of collagen type II caused by pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) is one of the major pathological characteristics of osteoarthritis (OA). Dimethyl fumarate (DMF) is a medication approved by the US Food and Drug Administration (FDA) as an oral multiple sclerosis (MS) therapy. In this study, we found that DMF ameliorated collagen type II degradation by inhibiting the expression of MMP-1, MMP-3, and MMP-13 caused by TNF-α. Mechanistically, DMF attenuated MMPs expression by suppressing JAK/STAT3 pathway. These findings imply that DMF treatment might be a potential therapeutic strategy for chondroprotective therapy.
