Department of Orthopedics, Shaoxing People's Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), Shaoxing, China.
Department of Orthopedics, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Front Endocrinol (Lausanne). 2022 Jul 22;13:926934. doi: 10.3389/fendo.2022.926934. eCollection 2022.
Osteoarthritis (OA) is a common degenerative joint condition associated with inflammation and characterized by progressive degradation of the articular cartilage and subchondral bone loss in the early stages. Inflammation is closely associated with these two major pathophysiological changes in OA. Velutin, a flavonoid family member, reportedly exerts anti-inflammatory effects. However, the therapeutic effects of velutin in OA have not yet been characterized. In this study, we explore the effects of velutin in an OA mouse model. Histological staining and micro-CT revealed that velutin had a protective effect against cartilage degradation and subchondral bone loss in an OA mouse model generated by surgical destabilization of the medial meniscus (DMM). Additionally, velutin rescued IL-1β-induced inflammation in chondrocytes and inhibited RANKL-induced osteoclast formation and bone resorption . Mechanistically, the p38 signaling pathway was found to be implicated in the inhibitory effects of velutin. Our study reveals the dual protective effects of velutin against cartilage degradation and subchondral bone loss by inhibiting the p38 signaling pathway, thereby highlighting velutin as an alternative treatment for OA.
骨关节炎（OA）是一种常见的退行性关节疾病，与炎症有关，其特征是在早期阶段关节软骨进行性退化和软骨下骨丢失。炎症与 OA 的这两个主要病理生理变化密切相关。Velutin 是黄酮类家族的一员，据报道具有抗炎作用。然而，Velutin 在 OA 中的治疗效果尚未得到描述。在这项研究中，我们探索了 Velutin 在 OA 小鼠模型中的作用。组织学染色和 micro-CT 显示，Velutin 对内侧半月板（DMM）手术不稳定引起的 OA 小鼠模型中的软骨降解和软骨下骨丢失具有保护作用。此外，Velutin 挽救了 IL-1β 诱导的软骨细胞炎症，并抑制了 RANKL 诱导的破骨细胞形成和骨吸收。机制上，发现 p38 信号通路参与了 Velutin 的抑制作用。我们的研究揭示了 Velutin 通过抑制 p38 信号通路对软骨降解和软骨下骨丢失的双重保护作用，从而强调了 Velutin 作为 OA 的一种替代治疗方法的潜力。
