miR‐382‐3p suppressed IL‐1β induced inflammatory response of chondrocytes via the TLR4/MyD88/NF‐κB signaling pathway by directly targeting CX43

miR‐382‐3p has been reported to be upregulated in synovial membrane in knee osteoarthritis (OA). Nevertheless, its role in OA remains largely unknown. The aim of this study was to investigate the specific function and mechanisms of miR‐382‐3p in the course of OA. In this study, human OA chondrocytes were pretreated with interleukin‐1β (IL‐1β) at 5 ng/ml for 12 hr to stimulate inflammatory response and matrix metalloproteinases (MMPs) expression in chondrocytes. Meanwhile, miR‐382‐3p was downregulated in IL‐1β‐stimulated chondrocytes. In addition, we found that miR‐382‐3p directly interacts with connexin 43 (CX43) and attenuates the increase of cytochrome c oxidase polypeptide II, inducible nitric oxide synthase, and MMP‐1/13 that is induced by IL‐1β. Furthermore, our observations indicated that miR‐382‐3p inhibited the expression of Toll‐like receptor 4 (TLR4), Myeloid differentiation primary response 88 (MyD88) and nuclear factor κB (NF‐κB) in IL‐1β‐stimulated chondrocytes, while CX43 overexpression could partly reverse these decreases. In conclusion, miR‐382‐3p participated in OA may through the TLR4/MyD88/NF‐κB signaling pathway by directly targeting CX43. miR‐382‐3p suppressed interleukin‐1β induced inflammatory response in chondrocytes via the Toll‐like receptor 4/Myeloid differentiation primary response 88/nuclear factor κB (TLR4/MyD88/NF‐κB) signaling pathway by directly targeting connexin 43 (CX43). miR‐382‐3p directly targeted CX43 messenger RNA, and inhibited the expression of CX43 protein, which further depressed the expression of TRL4, resulting in a deactivated TLR4/MyD88/NF‐κB signaling pathway.