Temporomandibular joint osteoarthritis (TMJ OA) is a complex multifactorial disease that can be induced by inflammation and oxidative stress. Curcumin has been reported to have anti-inflammatory and antioxidant properties. Herein, the anti-inflammatory and antioxidant mechanisms of curcumin in TMJ OA were investigated. Curcumin treatment inhibited the expression of the inflammation mediators IL-6, iNOS, and COX-2 and of the matrix-degrading proteinases MMP-1, MMP-3, MMP-9, MMP-13, ADAMTS-4, and ADAMTS-5 and upregulated the mRNA levels of the cartilage anabolic factors COL2A1 and ACAN after IL-1β treatment. Curcumin treatment also decreased oxidative stress injury following IL-1β stimulation. Pathway analysis demonstrated that the ROS/Nrf2/HO-1-SOD2-NQO-1-GCLC signaling axis is a key axis through which curcumin activates the Nrf2/ARE pathway in TMJ inflammatory chondrocytes. Curcumin-induced anti-inflammatory and cartilage protective effects were significantly abrogated by specific Nrf2 siRNA. In vivo results demonstrated that curcumin treatment protected TMJ articular cartilage from progressive degradation. Our experimental results indicate that curcumin inhibits inflammation, oxidative stress, and the matrix degradation of TMJ inflammatory chondrocytes through the Nrf2/ARE signaling pathway, thereby exerting cartilage protective effects. This study provides insight into potential therapeutic approaches for TMJ OA.

中文翻译：

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Nrf2 / ARE是姜黄素介导的TMJ软骨细胞免于氧化应激和炎症的关键途径。

颞下颌关节骨关节炎（TMJ OA）是一种复杂的多因素疾病，可以由炎症和氧化应激诱导。据报道姜黄素具有抗炎和抗氧化特性。本文研究了姜黄素在TMJ OA中的抗炎和抗氧化机理。姜黄素治疗抑制炎症介质IL-6，iNOS和COX-2以及基质降解蛋白酶MMP-1，MMP-3，MMP-9，MMP-13，ADAMTS-4和ADAMTS-5的表达IL-1β治疗后软骨合成代谢因子COL2A1和ACAN的mRNA水平上调。姜黄素治疗还可以降低IL-1β刺激后的氧化应激损伤。途径分析表明，ROS / Nrf2 / HO-1-SOD2-NQO-1-GCLC信号转导轴是姜黄素激活TMJ炎性软骨细胞中Nrf2 / ARE途径的关键轴。姜黄素诱导的抗炎和软骨保护作用被特定的Nrf2 siRNA大大废除了。体内结果表明姜黄素治疗可保护TMJ关节软骨免于进行性降解。我们的实验结果表明姜黄素通过Nrf2 / ARE信号通路抑制炎症，氧化应激和TMJ炎性软骨细胞的基质降解，从而发挥软骨保护作用。这项研究为TMJ OA的潜在治疗方法提供了见识。姜黄素诱导的抗炎和软骨保护作用被特定的Nrf2 siRNA大大废除了。体内结果表明姜黄素治疗可保护TMJ关节软骨免于进行性降解。我们的实验结果表明姜黄素通过Nrf2 / ARE信号通路抑制炎症，氧化应激和TMJ炎性软骨细胞的基质降解，从而发挥软骨保护作用。这项研究为TMJ OA的潜在治疗方法提供了见识。姜黄素诱导的抗炎和软骨保护作用被特定的Nrf2 siRNA大大废除了。体内结果表明姜黄素治疗可保护TMJ关节软骨免于进行性降解。我们的实验结果表明姜黄素通过Nrf2 / ARE信号通路抑制炎症，氧化应激和TMJ炎性软骨细胞的基质降解，从而发挥软骨保护作用。这项研究为TMJ OA的潜在治疗方法提供了见识。Nrf2 / ARE信号通路使TMJ炎性软骨细胞的基质降解，从而发挥软骨保护作用。这项研究为TMJ OA的潜在治疗方法提供了见识。Nrf2 / ARE信号通路使TMJ炎性软骨细胞的基质降解，从而发挥软骨保护作用。这项研究为TMJ OA的潜在治疗方法提供了见识。