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. 2023 Jun 1;13(9):3782–3801. doi: 10.1016/j.apsb.2023.05.034

Figure 4.

Figure 4

SMU-Y6 blocked the activation of TLR2/MyD88/NF-κB and MAPK signaling pathway and differential gene expression of seq-RNA analysis. (A) SMU-Y6 inhibited the upregulation of TLR2 induced by Pam3CSK4 (300 ng/mL) and SMU-Z1 (1 μmol/L) in HEK-blue hTLR2 cells. (B) SMU-Y6 inhibited the up-regulation of TLR2 and MyD88 induced by Pam3CSK4 (300 ng/mL) in THP-1 cells. (C) Co-immunoprecipitation showed that SMU-Y6 inhibited the formation of TLR2 and MyD88 complex induced by TLR2 agonist. (D) Murine peritoneal macrophages were pre-treated for 1 h with medium (or SMU-Y6) and treated with Pam3CSK4 (300 ng/mL) for 15, 30, and 60 min in the presence of medium or SMU-Y6. IB was performed using whole-cell lysates. (E) SMU-Y6 did not inhibit the up-regulation of TLR4 induced by LPS (100 ng/mL) in THP-1 cells. (F) Volcano plot exhibited genes differentially expressed (determined by RNA-seq analysis) in untreated THP-1 cells compared to SMU-Y6 treated cells and GSEA enrichment analysis shows variation in signaling pathway after SMU-Y6 treatment, noting that MAPK signaling pathway was involved. (G) Heatmap showed the expression of inflammation-associated genes on the treatment of SMU-Y6 among GSEA enrichment signaling pathway. The gene expression data were assessed by RNA-seq array.

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