LncRNA NUTM2A-AS1 调控miR-183-Sp/TGFa 影响骨 关节炎软骨细胞增殖、凋亡的研究.

Objective To explore the effect of LncRNA NUTM2A-AS I on interleukin-I 13 (IL-I 13) -induced chondrocyte damage and its molecular mechanism. Methods Chondrocytes were randomly divided into control group, model group (5 μg/ L IL-I 13 ), miR-183-Sp+model group, miR-NC+model group, si-LncRNA NUTM2A-ASl+model group, si-TGFa+model group, si-NC+ model group, pcDNA-TGFa+si-LncRNA NUTM2A-ASI +model group, pcDNA+si-LncRNA NUTM2A-ASI +model group; realtime fluorescent quantitative PCR (RT-qPCR ) was used to detect the expression levels of LncRNA NUTM2A-AS1, miR-183-Sp and TGFa mRNA; cell counting kit 8 ( CCK-8 ) was used to detect cell viability; flow cytometry was used to detect chondrocyte apoptosis; enzyme-linked immunosorbent assay ( ELISA) was used to detect the levels of TNF-a and IL-6; dual luciferase reporter experiment was used to detect the targeting relationship between NUTM2A-AS1, miR-183-Sp, and TGFa. Results In IL-113- induced chondrocytes, the expressions of LncRNA NUTM2A-AS I and TGFa were increased, the expression of miR-183-Sp was decreased, the activity of chondrocytes was decreased, the apoptosis rate was increased, and the levels of TNF-a and IL-6 were increased. Low expression of LncRNA NUTM2A-AS1, low expression of TGFa or overexpression of miR-183-Sp could promote cell proliferation and inh伽t apoptosis and inflammatory responses. Conclusion The low expression of LncRNA NUTM2A-AS I can inhibit IL-1[3-induced chondrocyte apoptosis and inflammation by regulating miR-183-Sp/TGFa, and promote cell survival. [ABSTRACT FROM AUTHOR]