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lncRNA NEAT1/SFPQ/RUNX2轴研究P-15对骨关节炎软骨损伤的保护作用 |
LncRNA NEAT1/SFPQ/RUNX2 axis study on the protective effect of P-15 on cartilage injury in osteoarthritis |
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DOI:10.3969/j.issn.1006-7108.2023.12.006 |
中文关键词: P-15肽 lncRNA NEAT1/SFPQ/RUNX2轴 人骨关节炎软骨细胞 凋亡 自噬 |
英文关键词:P-15 peptide lncRNA NEAT1/SFPQ/RUNX2 axis osteoarthritis chondrocytes apoptosis autophagy |
基金项目:2022年度川北医学院附属医院科研发展计划项目(2022JC008) |
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中文摘要: |
目的 探究P-15对人骨关节炎软骨细胞(HC-OA)的保护作用及与lncRNA NEAT1/SFPQ/RUNX2轴的关系。方法 分离HC-OA胞核、胞质RNA,RT-qPCR检测lncRNA NEAT1在细胞中的分布;P-15处理HC-OA细胞,转染siRNA NC和siRNA SFPQ后,RT-qPCR检测lncRNA NEAT1表达水平;流式细胞仪检测细胞凋亡;Western blot 检测RUNX2、SFPQ、Beclin-1、LC3B和P62表达水平。结果 lncRNA NEAT1同时存在于HC-OA胞质和胞核,且更多分布于细胞核;P-15可降低胞内lncRNA NEAT1水平(P<0.05),抑制骨关节炎软骨细胞凋亡(P<0.05);P-15可通过调控lncRNA NEAT1/SFPQ/RUNX2轴上调SFPQ表达和抑制RUNX2表达(P<0.01);P-15调控lncRNA NEAT1/SFPQ/RUNX2轴促进软骨细胞发生自噬(P<0.05)。结论 P-15可调控lncRNA NEAT1/SFPQ/RUNX2轴抑制HC-OA凋亡并促进自噬,保护软骨细胞免受损伤。 |
英文摘要: |
Objective To investigate the protective effect of P-15 on human osteoarthritic chondrocytes (HC-OA) and its relationship with lncRNA NEAT1/SFPQ/RUNX2 axis. Methods Nuclear and cytoplasmic RNAs of HC-OA were isolated, and the distribution of lncRNA NEAT1 in HC-OA cells was detected by RT-qPCR; HC-OA cells were treated with P-15 and transfected with siRNA NC and siRNA SFPQ, and the expression levels of lncRNA NEAT1 were detected by RT-qPCR; apoptosis was detected by flow cytometry; and the expression levels of RUNX2, SFPQ, Beclin-1, LC3B and P62 were detected by Western blot. Result lncRNA NEAT1 was present in both the cytoplasm and nucleus of HC-OA, and was more distributed in the nucleus; P-15 could reduce the intracellular lncRNA NEAT1 level (P<0.05) and inhibit osteoarthritis chondrocyte apoptosis (P<0.05); P-15 could up-regulate SFPQ expression and inhibit RUNX2 expression by regulating the lncRNA NEAT1/SFPQ/RUNX2 axis (P<0.01); P-15 regulated the lncRNA NEAT1/SFPQ/RUNX2 axis to promote autophagy in chondrocytes (P<0.05). Conclusion P-15 can regulate lncRNA NEAT1/SFPQ/RUNX2 axis to inhibit HC-OA apoptosis and promote autophagy, and protect chondrocytes from injury. |
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