The aim of the present study was to determine the function of microRNA (miR)-125b-5p in lumbar disc degeneration (LDD). Nucleus pulposus (NP) cells were stimulated with 10 ng/ml IL-1β for 24 h to establish an LDD model. Reverse transcription-quantitative PCR was used to assess miR-125b-5p levels in human lumbar degenerative NP samples and IL-1β-treated NP cells. An interaction between miR-125b-5p and TP53-regulated inhibitor of apoptosis 1 (TRIAP1) was revealed by TargetScan 7.1 and dual-luciferase reporter assay. Protein levels of pro-inflammatory factors were determined using ELISA. Cell viability and apoptosis were evaluated by MTT and flow cytometry analysis, respectively. miR-125b-5p was markedly upregulated in both human lumbar degenerative NP specimens and IL-1β-treated NP cells. TRIAP1, which directly targets miR-125b-5p, was markedly downregulated in human lumbar degenerative NP specimens and IL-1β-treated NP cells. The levels of TNF-α and IL-6 were inhibited in IL-1β-treated NP cells transfected with miR-125b-5p inhibitor. Moreover, miR-125b-5p inhibitor increased NP cell viability, prevented apoptosis and repressed the apoptotic peptidase activating factor 1/caspase 9 pathway in IL-1β-treated NP cells. Thus, the present findings suggested that miR-125b-5p could regulate LDD by adjusting NP cell apoptosis and inflammatory responses via TRIAP1.

本研究的目的是确定microRNA（miR）-125b-5p在腰椎间盘退变（LDD）中的功能。用10 ng / mlIL-1β刺激髓核（NP）细胞24小时，以建立LDD模型。使用逆转录定量PCR评估人腰部变性NP样品和IL-1β处理的NP细胞中的miR-125b-5p水平。通过TargetScan 7.1和双荧光素酶报告基因分析揭示了miR-125b-5p与TP53调节的凋亡抑制剂1（TRIAP1）之间的相互作用。使用ELISA确定促炎因子的蛋白质水平。通过MTT和流式细胞仪分析分别评估细胞活力和凋亡。在人类腰部变性NP标本和IL-1β处理的NP细胞中，miR-125b-5p均显着上调。直接针对miR-125b-5p的TRIAP1，在人类腰部变性NP标本和经IL-1β处理的NP细胞中，其明显下调。在用miR-125b-5p抑制剂转染的IL-1β处理的NP细胞中，TNF-α和IL-6的水平受到抑制。而且，miR-125b-5p抑制剂可提高IL-1β处理的NP细胞中NP细胞的活力，防止细胞凋亡并抑制凋亡肽酶激活因子1 / caspase 9途径。因此，本研究结果表明miR-125b-5p可以通过调节NP细胞凋亡和通过TRIAP1引起的炎症反应来调节LDD。在IL-1β处理的NP细胞中，它可以防止细胞凋亡并抑制凋亡肽酶激活因子1 / caspase 9通路。因此，本研究结果表明miR-125b-5p可以通过调节NP细胞凋亡和通过TRIAP1引起的炎症反应来调节LDD。在IL-1β处理的NP细胞中，它可以防止细胞凋亡并抑制凋亡肽酶激活因子1 / caspase 9通路。因此，本研究结果表明miR-125b-5p可以通过调节NP细胞凋亡和通过TRIAP1引起的炎症反应来调节LDD。