Abstract:Objective To explore the regulatory effect of Fuling Xingren Gancao granule (FXG) on macrophage polarization in atherosclerosis (AS) mice. Methods ApoE -/- mice were used to construct an AS model, while RAW264.7 macrophages were used to construct a polarized model. Oil red O and hematoxylin eosin staining (HE) were used to observe the total area of aortic plaques and the degree of aortic stenosis. PCR and Western blot were used to detect the expression levels, signal transduction, and transcription of M1 polarization factor inducible nitric oxide synthase (iNOS), monocyte chemotactic protein 1 (CCL2), M2 polarization factor arginase-1 (Arg-1), chitinase like protein 3 (YM1), and mannose receptor 1 (Mrcl or CD206) in vitro and in vivo. The phosphorylation level of signal transducer and activator of transcription (STAT3). Result: FXG significantly reduced the total area of aortic plaques in ApoE -/- mice, decreased the expression levels of M1 macrophage polarization factors iNOS and CCL2, and increased the expression levels of M2 macrophage polarization factors Arg-1 and YM1 (P<0.05). The phosphorylation levels of STAT3 in the model group mice and M1 macrophages decreased, but were upregulated after FXG intervention (P<0.05). The P-STAT3 inhibitor Stattic partially eliminated the regulatory effect of FXG on iNOS and Arg-1 (P<0.05).Result FXG significantly reduced the total area of aortic plaques in ApoE -/- mice, decreased the expression levels of M1 macrophage polarization factors iNOS and CCL2, and increased the expression levels of M2 macrophage polarization factors Arg-1 and YM1 (P<0.05). The phosphorylation levels of STAT3 in the model group mice and M1 macrophages decreased, but were upregulated after FXG intervention (P<0.05). The P-STAT3 inhibitor Stattic partially eliminated the regulatory effect of FXG on iNOS and Arg-1 (P<0.05).Conclusion FXG has an inhibitory effect on the progression of AS, which is related to the targeted regulation of macrophage polarization by STAT3.