YW3-56 reversed LPS-induced upregulation of inflammation-related genes. (A) There were 1789 genes in the intersection of upregulated genes in LPS relative to control samples and downregulated genes of LPS and YW3-56 dual treatment relative to LPS treatment samples. (B) These 1789 genes were mainly enriched for biological processes such as positive regulation of cytokine production, cytokine-mediated signaling pathway, etc., and enriched for molecular functions including cytokine and cytokine receptor activity, chemokine and chemokine receptor activity, etc. (C) These 1789 genes were enriched in KEGG functional pathways including cytokine-cytokine receptor interaction, TNF signaling, JAK-STAT signaling, NF-kappa B signaling, IL-17 signaling etc. (D) The upregulated cytokines (Il1a, Il1b, Il1rn, Il1f9, Il6, Il12a, Il15, Il17c, Il23a, Ifnb1, Ifng, Csf3, Lif, Osm, Gdf2, Gdf5, Gdf15, Inhbb) and cytokines receptor (Il1r1, Il1r2, Il2rb, Il12rb2, Il13ra1, Il15ra, Il17ra, Osmr, Edar), chemokines (Ccl3, Ccl4, Ccl5, Ccl11, Ccl17, Ccl19, Ccl20, Ccl22, Ccl28, Cxcl1, Cxcl2, Cxcl3, Cxcl5, Cxcl9, Cxcl10, Cxcl11, Cxcl14, Cxcl17) and chemokines receptors (Ccr7, Ccr8), NF-kappa B, IL-17 and Toll-like receptor signaling pathway genes (Nfkbia, Myd88, Lbp, Traf6) were reversed by YW3-56. The upregulated neutrophil marker genes (Elane, Mpo, Ly6g) caused by LPS were also reversed by YW3-56. (E) Quantitative-PCR analysis confirmed that the upregulated gene expression by LPS, including Il6, Ccl2, Cxcl9, Cxcl10, Nfkbia, and Elane. was reversed by YW3-56 (n ≥ 3). All data in figures were presented as mean ± SEM. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.