Notoginsenoside R1 suppresses inflammatory response and the pyroptosis of nucleus pulposus cells via inactivating NF-κB/NLRP3 pathways.

Intervertebral disc degeneration (IVDD) is the main cause of low back pain. Notoginsenoside R1 (NR1) is widely applied in the treatment of bone disorders, including IVDD. The present study aimed to investigate the effects of NR1 on the development of IVDD and the potential mechanisms. AF puncture was performed to establish IVDD rat model. Histology changes were analyzed by hematoxylin and eosin (H&E) staining. mRNA expressions were determined using qRT-PCR. Protein expressions were detected with western blot. Cellular functions were detected by MTT, EdU, flow cytometry, and TUNEL assays. The results showed that NR1 suppressed AF puncture induced IVDD, restored intervertebral disc (IVD) function, and suppressed mechanical hyperalgesia and thermal hyperalgesia. Moreover, NR1 promoted the release of extracellular matrix (ECM) in vivo and in vitro, and decreased the mRNA expressions of proinflammation cytokines. Additionally, NR1 inactivated NF-κB/NLRP3 pathways, improved cellular functions of nucleus pulposus cells (NPCs), and suppressed cell pyroptosis, which was reversed by NLRP3 activation. Taken together, NR1 may protect against IVDD via suppressing NF-κB/NLRP3 pathways. This may provide a novel therapy for IVDD.