Overproduction　of　reactive　oxygen　species　(ROS),　elevated　synovial　inflammation,　synovial　hyperplasia　and　fibrosis　are　the　main　characteristic　of　microenvironment　in　rheumatoid　arthritis　(RA).　Macrophages　and　fibroblast-like　synoviocytes　(FLSs)　play　crucial　roles　in　the　progression　of　RA.　Hence,　synergistic　combination　of　ROS　scavenging,　macrophage　polarization　from　pro-inflammatory　M1　phenotype　towards　M2　anti-inflammatory　phenotype,　and　restoring　homeostasis　of　FLSs　will　provide　a　promising　therapeutic　strategy　for　RA.　In　this　study,　we　successfully　synthesized　metformin-derived　carbon　dots　(MCDs),　and　investigated　the　antirheumatic　effect　in　vivo　and　in　vitro.　Designed　MCDs　could　target　inflamed　cells　and　accumulate　at　the　inflammatory　joints　of　collagen-induced　arthritis　(CIA)　rats.　In　vivo　therapeutic　investigation　suggested　that　MCDs　reduced　synovial　inflammation　and　hyperplasia,　ultimately　prevented　cartilage　destruction,　bone　erosion,　and　synovial　fibrosis　in　CIA　rats.　In　addition,　MCDs　eliminated　the　cellular　ROS　in　M1　phenotype　macrophages　in　RA　microenvironment　through　the　enzyme-like　catalytic　activity　as　well　as　inhibiting　NOD-like　receptor　family,　pyrin　domain　containing　3　(NLRP3)　inflammasome　signaling　pathway,　effectively　polarizing　them　into　the　M2　phenotype　to　realize　the　anti-inflammatory　effect.　Furthermore,　MCDs　could　inhibit　the　proliferation,　migration,　and　fibrosis　of　inflamed　FLSs.　Mechanistically,　MCDs　restored　the　homeostasis　of　FLSs　while　reducing　the　level　of　synovial　inflammation　by　blocking　IL-6/gp130　signaling　pathway.　Combined　with　preferable　biocompatibility,　MCDs　offer　a　prospective　treatment　approach　for　RA.