Background
As a common joint disease, osteoarthritis (OA) is the main cause of limited joint mobility and disability. The role of lncRNAs in the regulation of OA is increasingly discovered. Therefore, further exploring the function of SNHG7 in OA is of great significance for understanding its occurrence and development.
Conclusions
Collectively, The above results confirmed that SNHG7 prevents IL-1β induced OA by inhibiting NLRP3 inflammasome and apoptosis through miR-214-5p/PPARGC1B axis.
Methods
We used interleukin-1β (IL-1β) to treat to establish an OA model primary on chondrocytes in vitro, and gain- and loss of function assays of SNHG7 and miR-214-5p were conducted. The cell viability and apoptosis of chondrocytes were detected by CCK8 assay, BrdU assay and flow cytometry. The inflammatory cytokines (IL-1β, IL-6 and TNF-α), NLRP3 inflammasome, protein level of PPARGC1B, PPARγ, P38 and NF-κB were determined by RT-PCR and/or western blot.
Results
The results showed that SNHG7 was distinctly downregulated, while miR-214-5p was significantly upregulated in OA patients and primary chondrocytes treated with IL-1β. In addition, SNHG7 enhanced cell viability, inhibited apoptosis and inflammation of IL-1β-mediated chondrocytes. In contrast, miR-214-5p upregulation reduced viability, promoted apoptosis and inflammation of chondrocytes. Mechanistically, SNHG7 served as a competitive endogenous RNA by sponging miR-214-5p, which targeted PPARGC1B. Besides, the results of the compensation experiment affirmed that miR-214-5p attenuates SNHG7-mediated protective effects on IL-1β-mediated chondrocytes against apoptosis and inflammation, and activating PPARγ pathway markedly dampened the cytotoxic effects of miR-214-5p. Conclusions: Collectively, The above results confirmed that SNHG7 prevents IL-1β induced OA by inhibiting NLRP3 inflammasome and apoptosis through miR-214-5p/PPARGC1B axis.