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. Annexin Ⅴ- 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-1 β 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-1 β 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.