Yang Xiao, Li Baixing, Tian Haijun, Cheng Xiaofei, Zhou Tangjun, Zhao Jie
Shanghai Key Laboratory of Orthopedic Implants, Department of Orthopedics, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Front Pharmacol. 2022 Jun 20;13:905966. doi: 10.3389/fphar.2022.905966. eCollection 2022.
Low back pain (LBP) caused by intervertebral disc degeneration (IVDD) is accredited to the release of inflammatory cytokines followed by biomechanical and structural deterioration. In our study, we used a plant-derived medicine, curcumenol, to treat IVDD. A cell viability test was carried out to evaluate the possibility of using curcumenol. RNA-seq was used to determine relative pathways involved with curcumenol addition. Using TNFα as a trigger of inflammation, the activation of the NF-κB signaling pathway and expression of the MMP family were determined by qPCR and western blotting. Nucleus pulposus (NP) cells and the rats' primary NP cells were cultured. The catabolism status was evaluated by an model. A lumbar instability mouse model was carried out to show the effects of curcumenol . In general, RNA-seq revealed that multiple signaling pathways changed with curcumenol addition, especially the TNFα/NF-κB pathway. So, the NP cells and primary NP cells were induced to suffer inflammation with the activated TNFα/NF-κB signaling pathway and increased expression of the MMP family, such as MMP3, MMP9, and MMP13, which would be mitigated by curcumenol. Owing to the protective effects of curcumenol, the height loss and osteophyte formation of the disc could be prevented in the lumbar instability mouse model .
由椎间盘退变（IVDD）引起的下腰痛（LBP）被认为是炎症细胞因子释放后，继发生物力学和结构恶化所致。在我们的研究中，我们使用了一种植物源药物莪术烯醇来治疗IVDD。进行细胞活力测试以评估使用莪术烯醇的可能性。RNA测序用于确定与添加莪术烯醇相关的相对途径。以TNFα作为炎症触发因子，通过qPCR和蛋白质印迹法测定NF-κB信号通路的激活和MMP家族的表达。培养髓核（NP）细胞和大鼠原代NP细胞。通过一种模型评估分解代谢状态。建立腰椎不稳小鼠模型以显示莪术烯醇的作用。总体而言，RNA测序显示添加莪术烯醇后多种信号通路发生变化，尤其是TNFα/NF-κB通路。因此，NP细胞和原代NP细胞被诱导通过激活的TNFα/NF-κB信号通路和MMP家族（如MMP3、MMP9和MMP13）表达增加而发生炎症，而莪术烯醇可减轻这种炎症。由于莪术烯醇的保护作用，在腰椎不稳小鼠模型中可预防椎间盘的高度丢失和骨赘形成。
