Osteoarthritis (OA) is a disease characterized by degeneration of the joint complex due to cartilage destruction. Fraxetin, a widely used and studied coumarin compound extracted from a traditional Chinese herb (Qin Pi), has shown anti-inflammatory and antioxidant properties, but its effects on OA have not been studied. In the present study, western blotting, immunofluorescence, and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) were used to evaluate the effects of fraxetin on IL-1β-induced apoptotic activity, inflammatory responses, and catabolism in rat chondrocytes. The results showed that fraxetin prevented IL-1β-induced apoptosis of chondrocytes and inhibited inflammatory mediator release by regulating the Toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88)/nuclear factor (NF)-κB pathway in chondrocytes. Additionally, fraxetin suppressed the upregulation of matrix metalloproteinase 13 (MMP13) and degradation of collagen II in the extracellular matrix (ECM). Moreover, the effects of fraxetin in vivo were assessed in a monosodium iodoacetate (MIA)-induced rat model of OA using hematoxylin and eosin (H&E) and Safranin O-fast green staining and magnetic resonance imaging (MRI). The results showed that fraxetin protected the cartilage against destruction. In conclusion, fraxetin could be a potential therapeutic for OA.

骨关节炎（OA）是一种由于软骨破坏导致关节复合物变性的疾病。Fraxetin是一种从中草药（秦皮）提取的香豆素化合物，被广泛使用和研究，它具有抗炎和抗氧化特性，但尚未研究其对OA的作用。在本研究中，蛋白质印迹，免疫荧光和末端脱氧核苷酸转移酶（TdT）dUTP缺口末端标记（TUNEL）用于评估法拉西汀对大鼠软骨细胞IL-1β诱导的凋亡活性，炎症反应和分解代谢的影响。 。结果表明，法拉西汀通过调节软骨细胞中的Toll样受体4（TLR4）/髓样分化主要反应88（MyD88）/核因子（NF）-κB途径，阻止IL-1β诱导的软骨细胞凋亡并抑制炎症介质的释放。 。此外，法拉西汀抑制基质金属蛋白酶13（MMP13）的上调和细胞外基质（ECM）中胶原II的降解。此外，法拉西汀的作用使用苏木精和曙红（H＆E）以及番红O型快速绿染和磁共振成像（MRI）在碘乙酸单钠（MIA）诱导的OA大鼠模型中评估体内活性。结果表明，法拉西汀可以保护软骨免受破坏。总之，法拉西汀可能是OA的潜在疗法。