Fig 1: Wogonin activated CPT1α expression by binding and promoting PPARα nuclear translocation. A) Gene ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enriched in differentially expressed genes in macrophages after wogonin treatment. B) Transcriptome analysis of PPAR signaling in wogonin‐treated peritoneal macrophages. log2‐based transformation on ratio fold change values was used, where red shading indicates upregulation and green indicates down‐regulation. For each group, n = 3. C) The protein level of CPT1α in the plaque macrophages from mice treated with wogonin was determined by coimmunostaining with CD68 and CPT1α, n = 10. Scale bar: 200 µm. D) The protein level of CPT1α in peritoneal macrophages from mice treated with wogonin was determined by western blotting, n = 3. E,F) The levels of CPT1α in RAW264.7 cells after wogonin treatment were detected by immunofluorescence staining (n = 10, Scale bar: 20 µm) and western blotting (n = 3). G,H) Nuclear displacement of PPARα was detected by immunofluorescence staining in plaque macrophages (n = 10, Scale bar: 200 µm) and peritoneal macrophages (n = 3, Scale bar: 20 µm). I,J) The expression of PPARα in whole and nuclear proteins of RAW264.7 cells was detected by western blotting after treatment with wogonin, n = 3. K) Molecular docking predicts the presence of binding targets for wogonin and PPARα to form stable compounds. L) Surface plasmon resonance assay for interaction of wogonin was passed over the Biacore chip surfaces immobilized with recombinant PPARα protein: Biacore diagram and estimated dissociation constant value (KD) for wogonin binding PPARα. Data are presented as mean ± SEM. p‐values are shown in the figure C,D,F,G,I,J) by One‐way ANOVA with Tukey's multiple comparisons test. *p < 0.05, **p < 0.01, and ***p < 0.001, significantly different as indicated.