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Chlorogenic acid mediates JAK-STAT1 and NF-κB pathways to promote M1 phenotype polarization in mouse bone marrow macrophages
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  • Lu Wang,
  • Jiuwang Yu,
  • Zhiheng Dong,
  • Sha Li,
  • Lidao Bao,
  • Lan Wu
Lu Wang
The Affiliated Hospital of Inner Mongolia Medical University
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Jiuwang Yu
The Affiliated Hospital of Inner Mongolia Medical University
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Zhiheng Dong
The Affiliated Hospital of Inner Mongolia Medical University
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Sha Li
The Affiliated Hospital of Inner Mongolia Medical University
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Lidao Bao
The Affiliated Hospital of Inner Mongolia Medical University
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Lan Wu
Inner Mongolia Medical University

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Abstract

Purpose: The aim of this study was to investigate the mechanism of the polarization response of CGA on mouse bone marrow-derived macrophages (BMDMs) towards the M1 phenotype in an in vitro model and to verify whether JAK-STAT1 and NF-κB are involved in the CGA induced polarization response of M1 macrophages. Results: The purity of F4/80 in BMDMs was >90% as determined by flow cytometry, and CGA significantly promoted the expression of MCHⅡ,CD80andCD86 molecules on the surface of BMDMs, upregulated the expression of M1 macrophage marker CCR7 (C-C chemokine receptor type7) (P < 0.05) and decreased the expression of M2 macrophage marker CD206. The expression of TNF-α, IL-6 and IL-12 mRNA was significantly increased in CGA treated BMDMs compared to the control group,while the expression of CD206,Chil3,IL-10 and Arg1 mRNA was significantly decreased (P < 0.05). 6 and IL-12 in BMDMs (P < 0.05); In an in vitro bacterial phagocytosis and killing assay, CGA increased the uptake of FITC-Dextran by BMDMs and decreased the number of bacterial survival in Escherichia coli and Staphylococcus aureus;In addition, iNOS, NF -κBp65 and JAK-STAT1 protein expression levels were significantly increased in BMDMs (P < 0.05). These data suggest that CGA for M1 phenotypic polarization and expression of associated cytokines is closely associated with activation of NF-κBp65 and JAK-STAT1. Conclusion: CGA induces polarization of BMDMs towards M1-type macrophages and inhibits the trend towards M2-type macrophages,which is regulated by mediating JAK-STAT1 and NF-κB signalin