Local joint inflammation plays an important role in the pathogenesis of temporomandibular joint (TMJ) osteoarthrosis (TMJOA). Yohimbine, an alpha-2 adrenergic receptor antagonist, possesses anti-inflammatory properties; however, the ability of Yohimbine to protect against TMJOA-associated chondrocyte inflammation remains unclear. We conducted in vitro and in vivo analyses to investigate whether Yohimbine could ameliorate TMJOA-induced chondrocyte inflammation and to elucidate the mechanisms involved. Chondrocytes of TMJOA mice were stimulated with interleukin (IL)-1β or noradrenaline (NE), and the resulting production of inflammation-related factors was evaluated in the presence or absence of Yohimbine. Furthermore, two TMJOA mouse models were treated with Yohimbine and the therapeutic effect was quantified. NE (10⁻⁶ M) triggered inflammatory cytokine secretion by TMJ chondrocytes, and Yohimbine suppressed IL-1β- or NE-induced IL-6 upregulation in TMJ chondrocytes with the nuclear factor (NF)–κB pathway inhibition. Yohimbine also ameliorated cartilage destruction in the TMJOA models. Interestingly, αmpT, a tyrosine hydroxylase inhibitor, reversed the effects of Yohimbine by activating the NF-κB pathway. Collectively, these findings show that Yohimbine ameliorated TMJ chondrocyte inflammation and the suppression of NF-κB pathway contributes to this effect.

局部关节炎症在颞下颌关节 (TMJ) 骨关节病 (TMJOA) 的发病机制中起重要作用。育亨宾是一种 α-2 肾上腺素能受体拮抗剂，具有抗炎特性；然而，育亨宾防止 TMJOA 相关软骨细胞炎症的能力仍不清楚。我们进行了体外和体内分析以研究育亨宾是否可以改善 TMJOA 诱导的软骨细胞炎症并阐明所涉及的机制。用白介素 (IL)-1β 或去甲肾上腺素 (NE) 刺激 TMJOA 小鼠的软骨细胞，并在存在或不存在育亨宾的情况下评估炎症相关因子的产生。此外，两个 TMJOA 小鼠模型用育亨宾治疗，并量化了治疗效果。东北 (10 ^-6M) 触发 TMJ 软骨细胞的炎性细胞因子分泌，育亨宾通过核因子 (NF)-κB 通路抑制抑制 IL-1β 或 NE 诱导的 TMJ 软骨细胞中的 IL-6 上调。育亨宾还改善了 TMJOA 模型中的软骨破坏。有趣的是，αmpT，一种酪氨酸羟化酶抑制剂，通过激活 NF-κB 通路来逆转育亨宾的作用。总的来说，这些发现表明育亨宾改善了 TMJ 软骨细胞炎症，NF-κB 通路的抑制有助于这种效果。