In this study, miR-19b-3p was downregulated in osteoarthritic cartilage tissues and IL-1β-stimulated primary chondrocytes, and miR-19b-3p overexpression reversed the inhibitory effect of IL-1β on cell viability, the promotion effects of apoptosis, inflammatory factor secretion and extracellular matrix degradation, whereas the opposite effect was observed with miR-19b-3p inhibitor. Moreover, SOCS1 is a target gene of miR-19b-3p. Furthermore, SOCS1 overexpression enhanced cell injury compared with IL-1β alone treatment, whereas knockdown of SOCS1 restored cell damage caused by IL-1β. Further studies revealed that miR-19b-3p promoted chondrocyte injury repair by suppressing SOCS1 expression, and we found that was mediated by blocking the MAPK/NF-κB axis. Taken together, our findings may provide a new therapeutic strategy for osteoarthritis.
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