Piceatannol inhibits the IL-1β-induced inflammatory response in human osteoarthritic chondrocytes and ameliorates osteoarthritis in mice by activating Nrf2

), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6)-but also suppressed the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) at both the mRNA and protein levels. Piceatannol also decreased the expression of metalloproteinase 13 (MMP13) and thrombospondin motifs 5 (ADAMTS5), which mediate extracellular matrix degradation. Mechanistically, we found that piceatannol inhibited IL-1β-induced nuclear factor kappa B (NF-κB) activation by activating the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway. Furthermore, piceatannol exerted protective effects in a mouse model of OA. Taken together, these findings indicate that piceatannol may be a potential therapeutic agent for OA.