Abstract
Curcumin, with its antioxidant, anti-inflammatory, and antitumor properties, is widely used in the treatment of bone disorders, including rheumatoid arthritis (RA). We investigated the effects of curcumin on fibroblast-like synoviocytes in RA and its underlying mechanism. mRNA and microRNA (miRNA) expression levels were determined using reverse transcription-quantitative polymerase chain reaction. Cellular functions were detected using cell counting kit-8, 5-ethynyl-2'-deoxyuridine, Transwell, and flow cytometric assays. Enzyme-linked immunosorbent assay was performed to measure the cytokine release. Western blotting was used to determine the protein expression levels. An in vivo assay was performed to verify the role of linc00052 in RA. Curcumin promoted apoptosis and inhibited the growth, migration, and invasion of RA fibroblast-like synovial (RAFLS) cells. Curcumin treatment suppressed the inflammatory response of RAFLS cells. Moreover, curcumin increased linc00052 levels, and linc00052 knockdown reversed the effects of curcumin. Additionally, linc00052 functioned as a competing endogenous RNA to upregulate the expression of the protein inhibitor of activated STAT 2 (PIAS2) by sponging miR-126-5p. Curcumin inhibited the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway. In vivo assays showed that curcumin decreased the arthritis score and improved inflammatory infiltration and synovial cell proliferation. These results reveal that curcumin protects against RA by regulating the inc00052/miR-126-5p/PIAS2 axis through JAK2/STAT3 signaling pathway.
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