LAUSR

Long noncoding RNAs serve as novel regulatory molecules involved in various biological processes, but their role in osteoarthritis (OA) remains unknown. Therefore, we aimed to reveal the inflammatory mechanisms regulated by CILinc02 and methylene blue in human osteoarthritic cartilage and to explore the potential functions of CILinc02 and methylene blue in OA. The expression level of CILinc02 in OA cartilage tissues and primary cells was obtained using quantitative reverse transcriptase polymerase chain reaction (qRT‐PCR). The cytokines, such as interleukin 1 (IL‐1), IL‐6, IL‐17, tissue inhibitor of metalloproteinase‐1 (TIMP‐1) and matrix metalloproteinase (MMPs), involved in the degradation of chondrocyte in CILinc02 knockdown OA primary cells, which were treated with methylene blue that were determined by enzyme‐linked immunosorbent assay, qRT‐PCR and Western blot analysis. The results showed that CILinc02 was overexpressed in osteoarthritic cartilage tissues and in OA primary cells, but methylene blue can inhibit the expression of CILinc02. In addition, overexpression of CILinc02 induced the inflammation and apoptosis in primary OA cells, however, the effect of methylene blue was reversed compared to CILinc02. Meanwhile, methylene blue can regulate the expression of TIMP‐1, MMP‐1, and MMP‐13 proteins, thereby suppressing the degradation of chondrocyte in OA. This evidence indicates that methylene blue can act as an inflammatory inhibitor by targeting CILinc02 to regulate the inflammatory response.