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.

椎间盘退变（IVDD）是腰痛的主要原因。三七皂甙 R1 (NR1) 广泛用于治疗骨疾病，包括 IVDD。本研究旨在探讨 NR1 对 IVDD 发展的影响及其潜在机制。AF穿刺建立IVDD大鼠模型。通过苏木精和伊红 (H&E) 染色分析组织学变化。使用 qRT-PCR 测定 mRNA 表达。用蛋白质印迹检测蛋白质表达。通过 MTT、EdU、流式细胞术和 TUNEL 测定检测细胞功能。结果表明，NR1抑制AF穿刺诱导的IVDD，恢复椎间盘（IVD）功能，抑制机械痛觉过敏和热痛觉过敏。此外，NR1促进细胞外基质（ECM）的释放体内外均显着降低促炎细胞因子的mRNA表达。此外，NR1 可灭活 NF-κB/NLRP3 通路，改善髓核细胞 (NPC) 的细胞功能，并抑制细胞焦亡，而 NLRP3 激活可逆转这种情况。总之，NR1 可以通过抑制 NF-κB/NLRP3 通路来预防 IVDD。这可能为 IVDD 提供一种新的治疗方法。