The etiology of lumbocrural pain is closely related to intervertebral disc degeneration (IDD). Long noncoding RNAs (lncRNAs) serve crucial roles in IDD progression. This study investigated the effect of lncRNA H19 on autophagy and apoptosis of nucleus pulposus cells (NPCs) in IDD. The rat model of IDD was established. Normal NPCs and degenerative NPCs (DNPCs) were cultured in vitro. H19 expression in IDD rat was detected. DNPCs were treated with si-H19 to evaluate autophagy and apoptosis of DNPCs. The binding relationships between H19 and miR-139-3p, and miR-139-3p and CXCR4 were verified. DNPCs were co-transfected si-H19 and miR-139-3p inhibitor. The phosphorylation of NF-κB pathway-related p65 in DNPCs was detected. LncRNA H19 was upregulated in IDD rats. Downregulation of H19 inhibited autophagy and apoptosis of DNPCs. LncRNA H19 sponged miR-139-3p to inhibit CXCR4 expression. si-H19 and miR-139-3p inhibitor co-treatment induced autophagy and apoptosis, and enhanced CXCR4 expression. si-H19 decreased p-p65 phosphorylation, while si-H19 and miR-139-3p inhibitor co-treatment partially elevated p-p65 phosphorylation. In conclusion, lncRNA H19 facilitated the autophagy and apoptosis of DNPCs by the miR-139-3p/CXCR4/NF-κB axis, thereby aggravating IDD. This study may offer new insights for the management of IDD.

中文翻译：

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LncRNA H19通过miR-139/CXCR4/NF-κB轴促进髓核细胞的自噬和凋亡，从而加重椎间盘退变

腰腿痛的病因与椎间盘退变（IDD）密切相关。长链非编码 RNA (lncRNA) 在 IDD 进展中起关键作用。本研究探讨了 lncRNA H19对 IDD 中髓核细胞 (NPCs) 自噬和凋亡的影响。建立IDD大鼠模型。体外培养正常 NPC 和退行性 NPC (DNPC)。检测IDD大鼠中的H19表达。用 si-H19 处理 DNPC 以评估 DNPC 的自噬和凋亡。验证了H19与miR-139-3p、miR-139-3p与CXCR4的结合关系。DNPCs 共转染 si-H19 和 miR-139-3p 抑制剂。检测到 DNPCs 中 NF-κB 通路相关 p65 的磷酸化。LncRNA H19在 IDD 大鼠中上调。H19的下调抑制了DNPC的自噬和凋亡。LncRNA H19海绵化 miR-139-3p 以抑制 CXCR4 表达。si-H19 和 miR-139-3p 抑制剂联合治疗可诱导自噬和细胞凋亡，并增强 CXCR4 的表达。si-H19 降低了 p-p65 磷酸化，而 si-H19 和 miR-139-3p 抑制剂联合处理部分提高了 p-p65 磷酸化。总之，lncRNA H19通过miR-139-3p/CXCR4/NF-κB轴促进了DNPCs的自噬和凋亡，从而加重了IDD。这项研究可能为 IDD 的管理提供新的见解。