Department of Orthopaedic Surgery, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109, Xueyuanxi road, 325027 Wenzhou, China.
Food Funct. 2017 Nov 15;8(11):3926-3937. doi: 10.1039/c7fo00822h.
Osteoarthritis (OA) is a complex process, to which an inflammatory environment contributes markedly. Piceatannol exerts anti-inflammatory effects on several diseases. In the current study, we explored the protective effects of piceatannol on the progression of OA and investigated its molecular target. In vitro, piceatannol not only attenuated the over-production of inflammatory mediators and cytokines-such as nitric oxide (NO), prostaglandin E2 (PGE), 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.
骨关节炎（OA）是一个复杂的过程，其中炎症环境有显著贡献。白皮杉醇对几种疾病具有抗炎作用。在目前的研究中，我们探讨了白皮杉醇对 OA 进展的保护作用，并研究了其分子靶标。在体外，白皮杉醇不仅减弱了炎症介质和细胞因子（如一氧化氮（NO）、前列腺素 E2（PGE2）、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6））的过度产生，还抑制了环氧化酶-2（COX-2）和诱导型一氧化氮合酶（iNOS）在 mRNA 和蛋白质水平的表达。白皮杉醇还降低了介导细胞外基质降解的基质金属蛋白酶 13（MMP13）和血小板反应蛋白基序 5（ADAMTS5）的表达。从机制上讲，我们发现白皮杉醇通过激活核因子（红细胞衍生 2）样 2（Nrf2）/血红素加氧酶 1（HO-1）途径抑制白细胞介素-1β诱导的核因子 kappa B（NF-κB）激活。此外，白皮杉醇在 OA 小鼠模型中发挥了保护作用。总之，这些发现表明白皮杉醇可能是 OA 的一种潜在治疗剂。
