Myricetin Exerts Anti-osteoarthritic Effects in IL-1β Stimulated SW1353 Cells via Regulating Matrix Metalloproteinases and Modulating JNK/P38MAPK/Ap-1/c-Fos and JAK/STAT Signalling

In arthritis, osteoarthritis (OA) is very common and is a progressive chronic illness of the joint impairing its function and thereby eventually affects the quality of patient's life. Currently employed therapeutic drugs aim to alleviate OA symptoms, however it poses adverse effects. Hence, identification of novel compounds that could effectively block the progression of OA and as well reduce symptoms is of high clinical value. This investigation was carried out to assess the effects a flavonoid, myricetin on the IL-1 beta induced SW1353 cells. The SW1353 cells were subjected to myricetin treatment at 75, 150 or 300 mu g for 3 h before IL-1 beta stimulation at 5 ng mL(-1) for 24 h and the treatment with myricetin significantly improved the cell viability of IL-1 beta-induced SW1353 cells and reduced the levels of PGE2 and NO. The results suggest the anti-inflammatory effects of myricetin. In addition, myricetin effectively supressed matrix metalloproteinases (MMPs-MMP1, 3 and 13) expression and also the expression of mitogen activated protein kinases (ERK, JNK and p38 kinase). The activation of NF-kappa B and AP-1 (transcription factors) were regulated by myricetin. Further, JAK2/STAT1 signalling was modulated effectively on myricetin treatment at all the three tested doses in a concentration dependent manner. Myricetin thus by targeting major pathways in pathogenesis of OA could be explored further for its therapeutic potential in OA treatment.