Background/aims:　Rheumatoid　arthritis　synovial　fibroblasts　(RASF)　play　an　essential　role　in　the　pathogenesis　of　rheumatoid　arthritis　(RA).　This　study　aimed　to　investigate　the　biological　effects　of　miR-22　on　RASFs.　Methods:　RT-gPCR　was　used　to　detect　the　expressions　of　miR-22　and　SIRT1　in　RA　synovial　tissue.　The　results　of　miR-22　on　the　proliferation　of　RASF　were　examined　by　MTT　assay.　The　effects　of　miR-22　on　the　secretion　of　TNF-alpha,　IL-1　beta,　and　IL-6　in　RASF　were　measured　by　ELISA.　Target　gene　prediction　and　screening,　and　luciferase　reporter　assay　were　used　to　testify　downstream　target　genes　of　miR-22.　RT-gPCR　and　western　blotting　were　used　to　detect　the　mRNA　and　protein　expression　of　SIRT1.　Results:　miR-22　was　significantly　decreased　in　RA　synovial　tissue,　while　SIRT1　was　significantly　increased　in　RA　synovial　tissue.　Over-expression　of　miR-22　significantly　inhibited　the　proliferation　of　RASFs　and　the　secretions　of　inflammatory　cytokines　(TNF-alpha,　IL-1　beta,　and　IL-6)　in　RASFs.　SIRT1　was　identified　as　a　direct　target　of　miR-22.　Over-expression　of　miR-22　reduced　the　expression　level　of　SIRT1　in　RASFs.　Over-expression　of　SIRT1　reversed　the　effect　of　miR-22　on　the　proliferation　of　RASFs　and　the　secretion　of　inflammatory　cytokines.　Conclusion:　MIR-22　was　significantly　down-regulated　in　BASF　cells,　which　affected　the　secretions　of　inflammatory　cytokines　and　cell　proliferation　by　regulating　SIRT1.