Key Laboratory of Drug-Targeting and Drug Delivery System of Sichuan Province, Sichuan Industrial Institute of Antibiotics, School of Pharmacy, Chengdu University, Chengdu 610106, China; School of Food and Biological engineering, Chengdu University, Chengdu 610106, China.
Key Laboratory of Drug-Targeting and Drug Delivery System of Sichuan Province, Sichuan Industrial Institute of Antibiotics, School of Pharmacy, Chengdu University, Chengdu 610106, China; School of Chemical Engineering, Sichuan University, Chengdu, 610065, Sichuan, China.
Cytokine. 2023 Sep;169:156309. doi: 10.1016/j.cyto.2023.156309. Epub 2023 Jul 28.
Osteoarthritis (OA) is a prevalent degenerative joint disorder caused by the progressive destruction of cartilage and inflammation in the articular cavity. Studies have proved that the inhibition of articular cartilage destruction and generation of inflammatory factors can be effective strategies for treating OA. Notopterol (NOT) is a quality control index of Notopterygium incisum Ting ex H. T. Chang (N. incisum) with anti-inflammatory, antioxidant, and analgesic activities. Moreover, NOT has been used for many years to treat joint diseases. A study using human C28/I2 cells suggested that NOT down-regulated the hypersecretion of inflammatory mediators and alleviated the degradation of the extracellular matrix (ECM). In addition, NOT decreased the overproduction of reactive oxygen species (ROS) and chondrocyte apoptosis through the nuclear factor erythroid-2-related factor 2 (Nrf2) signaling pathway. NOT exerted a chondroprotective effect by partly inhibiting the Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathways and regulating the nuclear factor Nrf2/heme oxygenase-1(HO-1) signaling pathway. In vivo, NOT improved the destruction of articular cartilage in a rat OA model, which may be related to the inhibition of tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, and IL-12 expressions in synovial fluid. In summary, these results showed that NOT alleviated the progression of OA and is expected to become a new therapy for treating OA clinically.
骨关节炎（OA）是一种常见的退行性关节疾病，由关节腔内软骨的进行性破坏和炎症引起。研究表明，抑制软骨破坏和炎症因子的产生是治疗 OA 的有效策略。羌活醇（NOT）是羌活（N. incisum）的质量控制指标，具有抗炎、抗氧化和镇痛作用。此外，NOT 多年来一直被用于治疗关节疾病。一项使用人 C28/I2 细胞的研究表明，NOT 下调了炎症介质的过度分泌，并缓解了细胞外基质（ECM）的降解。此外，NOT 通过核因子红细胞 2 相关因子 2（Nrf2）信号通路减少活性氧（ROS）的过度产生和软骨细胞凋亡。NOT 通过部分抑制 Janus 激酶 2/信号转导和转录激活因子 3（JAK2/STAT3）和磷脂酰肌醇 3-激酶/蛋白激酶 B（PI3K/AKT）信号通路，并调节核因子 Nrf2/血红素加氧酶-1（HO-1）信号通路发挥软骨保护作用。在体内，NOT 改善了大鼠 OA 模型中关节软骨的破坏，这可能与抑制滑液中肿瘤坏死因子α（TNF-α）、白细胞介素（IL）-1β、IL-6 和 IL-12 的表达有关。综上所述，这些结果表明 NOT 缓解了 OA 的进展，有望成为临床上治疗 OA 的一种新疗法。
