〔Abstract〕 Objective To explore the effects of long non-coding RNA(LncRNA) MIR22HG on proliferation, apoptosis and inflammatory response of rheumatoid arthritis(RA) fibroblast-like synoviocytes(FLSs) and its molecular mechanism. Methods Synovial tissue samples were collected from 37 RA patients and 30 joint trauma patients in our hospital, and the expression levels of MIR22HG and miR-22-5p in synovial tissue were detected by qRT-PCR. RA-FLSs in human was isolated, cultured and identified in vitro. MIR22HG siRNA interference plasmid (si-MIR22HG) and its negative control plasmid(si-NC),miR-22-5p inhibitor and its negative control(inhibitorNC) were transfected into RA-FLSs respectively or simultaneously. The expression levels of MIR22HG and miR-22-5p were detected by qRT-PCR. CCK-8 was used to detect the proliferation activity of cells in various groups.AnnexinⅤ-FITC/PI was used to detect the apoptosis rates of cells in various groups. ELISA was used to detect the levels of TNF-α,IL-1β and IL-6 in the supernatant of cells in various groups. Western blot was used to detect the protein expression levels of Bcl-2,Bax and Cleaved caspase-3 of cells in various groups. The targeting relationship between MIR22HG and miR-22-5p was verified by dual luciferase reporter gene assay. Results Compared with joint trauma patients,the expression level of MIR22HG in synovial tissues of RA patients increased(P<0. 05),while the expression level of miR-22-5p decreased(P<0. 05). Interference with MIR22HG inhibited the proliferation activity of RA-FLSs,decreased the levels of TNF-α,IL-1β and IL-6 in cell supernatant and the protein expression level of Bcl-2 in cells(P<0. 05),and increased the apoptosis rate,the expression level of miR-22-5p and the protein expression levels of Bax and Cleaved casepase-3(P<0. 05). However,inhibition of miR-22-5p expression reversed the effects of MIR22HG gene silencing on proliferation,apoptosis and inflammation of RA-FLSs(P<0. 05). Dual luciferase reporting assay showed that miR-22-5p was a potential downstream miRNA target of MIR22HG. Conclusion MIR22HG is highly expressed in synovial tissues of RA patients,and it may promote the proliferation and the inflammatory response of RA-FLSs and inhibit cell apoptosis by down regulating the expression of miR-22-5p.