Nucleus pulposus cell (NPC) is the major cell type maintaining the physiological function of intervertebral discs by producing extracellular matrix (ECM). NPC apoptosis and senescence together contribute to NPC loss, finally leading to intervertebral disc degeneration (IDD). Herein, miR-623 showed to be downregulated within IDD tissue samples according to both bioinformatics and experimental analyses. In LPS-injured NPCs, miR-623 overexpression promoted LPS-suppressed cell proliferation; moreover, miR-623 overexpression inhibited cell apoptosis and senescence, increased ECM secretion, and reduced levels of inflammatory factors. In contrast to miR-623, CXCL12 expression was significantly upregulated in IDD tissues; miR-623 directly bound CXCL12 to inhibit its expression. In LPS-stimulated NPCs, CXCL12 silencing also LPS-induced changes in cell proliferation, cell senescence, ECM secretion, and inflammatory factor levels. More importantly, CXCL12 overexpression aggravated LPS-induced changes and significantly reversed the protective effects of miR-623 overexpression. In conclusion, the miR-623/CXCL12 axis could affect NPC apoptosis and senescence, ECM deposition, and inflammatory factor levels under LPS stimulation in vitro. The p65 signaling might be involved.

髓核细胞（NPC）是通过产生细胞外基质（ECM）来维持椎间盘生理功能的主要细胞类型。NPC 细胞凋亡和衰老共同导致 NPC 丢失，最终导致椎间盘退变 (IDD)。在此，根据生物信息学和实验分析，miR-623 在 IDD 组织样本中被下调。在 LPS 损伤的 NPC 中，miR-623 过表达促进了 LPS 抑制的细胞增殖；此外，miR-623过表达抑制细胞凋亡和衰老，增加ECM分泌，降低炎症因子水平。与 miR-623 相比，IDD 组织中 CXCL12 的表达显着上调；miR-623 直接结合 CXCL12 以抑制其表达。在 LPS 刺激的 NPC 中，CXCL12 沉默还会引起 LPS 诱导的细胞增殖、细胞衰老、ECM 分泌和炎症因子水平的变化。更重要的是，CXCL12 过表达加重了 LPS 诱导的变化，并显着逆转了 miR-623 过表达的保护作用。综上所述，miR-623/CXCL12轴可影响LPS刺激下NPC细胞凋亡和衰老、ECM沉积和炎症因子水平体外。可能涉及 p65 信号。