Parmatine mediates the miR-361-3p/SOCS3 signaling axis affecting macrophage M1/M2 polarization and migration in sepsis

AimTo investigate the molecular mechanism by which palmatine regulates the polarization and migration of septic macrophages through the miR-361-3p/SOCS3 signaling axis.MethodsAn LPS-induced sepsis model in C57BL/6 mice was established. The mice were randomly divided into a control group (NC), a sepsis group (Sepsis), and a palmatine intervention group (palmatine, intraperitoneal injection at a dose of 25 mg·kg-1 for 14 days). The levels of serum inflammatory factors (IL-1β, TNF-α, IL-6)and renal pathological changes were detected by ELISA. The expressions of miR-361-3p and SOCS3 were analyzed by qRT-PCR and FISH. An in vitro sepsis model of bone marrow-derived macrophages (BMDMs) was constructed. The targeting relationship between miR-361-3p and SOCS3 was verified by dual-luciferase reporter gene assay. The expressions of SOCS3/p-NF-κB proteins and M1/M2 markers (iNOS/Arg-1) were detected, and the cell migration ability was evaluated.ResultsPalmatine significantly reduced the levels of serum IL-1β, TNF- α, and IL-6 in septic mice (P P 50 = 65. 91 nmo·L-1) inhibited the SOCS3/p-NF- κB pathway by activating miR-361- 3p, decreased the expression of the M1 polarization marker iNOS in BMDM cells (P P ConclusionPalmatine regulates the M1/M2 polarization balance of macrophages via the miR-361-3p/SOCS3 axis and suppresses the inflammatory response and cell migration, thus offering potential targets for the treatment of sepsis.