Inhibition of miR-126 protects chondrocytes from IL-1β induced inflammation via upregulation of Bcl-2

Objectives The aim of this study was to investigate the role of miR-126 in the development of osteoarthritis, as well as the potential molecular mechanisms involved, in order to provide a theoretical basis for osteoarthritis treatment and a novel perspective for clinical therapy. Methods Human chondrocyte cell line CHON-001 was administrated by different doses of interleukin (IL)-1 beta to simulate inflammation. Cell viability, migration, apoptosis, IL-6, IL-8, and tumour necrosis factor (TNF)-alpha expression, as well as expression of apoptosis-related factors, were measured to assess inflammation. miR-126 expression was measured by quantitative polymerase chain reaction (qPCR). Cells were then transfected with miR-126 inhibitor to assess the effect of miR-126 on IL-1 beta-injured CHON-001 cells. Expression of B-cell lymphoma 2 (Bcl2) and the activity of mitogen-activated protein kinase (MAPK) / Jun N-terminal kinase (JNK) signaling pathway were measured by Western blot to explore the underlying mechanism through which miR-126 affects IL-1 beta-induced inflammation. Results After IL-1 beta administration, cell viability and migration were suppressed while apoptosis was enhanced. Expression of IL-6, IL-8, and TNF-alpha were all increased, and miR-126 was upregulated. In IL-1 beta-administrated CHON-001 cells, miR-126 inhibitor suppressed the effect of IL-1 beta on cell viability, migration, apoptosis, and inflammatory response. Bcl-2 expression was negatively regulated with miR-126 in IL-1 beta-administrated cells, and thus affected expressions of phosphorylated MAPK and JNK. Conclusion IL-1 beta-induced inflammatory markers and miR-126 was upregulated. Inhibition of miR-126 decreased IL-1 beta-induced inflammation and cell apoptosis, and upregulated Bcl-2 expression via inactivating the MAKP/JNK signalling pathway.