miR‑27 inhibits the NF-κB signaling pathway by targeting leptin in osteoarthritic chondrocytes.

Osteoarthritis (OA) is a chronic degenerative joint disease. An increasing number of studies point to the role of microRNAs (miRNAs or miRs) in the pathogenesis of OA. An earlier study suggested that miR‑27b was associated with OA; however, the precise mechanisms regarding the involvement of the miR‑27 in the progression of OA remain unclear. In the present study, we first analyzed the effects of miR‑27 on OA. In vitro, the degree of miR‑27 expression was decreased in chondrocytes obtained from patients with OA. Transfection with miR‑27 mimic increased the viability of CH8 cells and induced the expression of type-II collagen, type-X collagen, glycosaminoglycan (GAG) and aggrecan (ACAN). The results of luciferase activity assay revealed that miR‑27 directly targeted the 3'-untranslated region (3'-UTR) of leptin. The results of western blot analysis and ELISA indicated that the concentration of leptin was decreased after the CH8 cells were transfected with miR‑27 mimic. In vivo, a rat model of OA was established by anterior cruciate ligament transection (ACLT). When the rats with OA were injected with miR‑27 lentiviral overexpression vector, the results of ELISA revealed that the levels of interleukin (IL)-6 and IL-8 were decreased. The results of western blot analysis revealed that matrix metalloproteinase (MMP)-9 and MMP-13 expression levels were decreased, and the nuclear factor-κB (NF-κB) pathway was inhibited. On the whole, our results suggest that the upregulation of miR‑27 inhibits the pathogenesis of OA by targeting leptin and inhibiting the NF-κB signaling pathway. Thus, miR‑27 exerts protective effects against OA.