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    Article

    Narirutin Suppresses M1‑Related Chemokine InterferonGamma-Inducible Protein‑10 Production in Monocyte‑Derived M1 Cells via Epigenetic Regulation

    Chung‑Hsiang Li1, Lin Wang2, Chang‑Hung Kuo3, Yi‑Ting Chen4, Mei‑Lan Tsai4, Chih‑Hsing Hung5★★ Corresponding author

    1. 1Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University, China.
    2. 2Department of Pediatrics, Po‑Jen Hospital, China.
    3. 3Ta‑Kuo Clinic, China.
    4. 4Department of Laboratory Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, China.
    5. 5Department of Pediatrics, Kaohsiung Municipal Siaoqang Hospital, Kaohsiung City, Republic of, China, Taiwan.

    CORRESPONDENCE

    Chih‑Hsing Hung

    Department of Pediatrics, Kaohsiung Municipal Siaoqang Hospital, Kaohsiung City, Republic of, China, Taiwan.

    pedhung@gmail.com

    Received: 19-03-2020; Revised: 20-04-2020; Accepted: 15-07-2020.

    Volume 16, Issue 71 · pp. 479–485 · PUBLISHED 20 October 2020 · DOI: 10.4103/pm.pm_105_20

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Objective: We try to investigate this anti‑inflammatory effect of narirutin in human monocytic THP‑1‑derived M1 macrophage cells. Materials and Methods: To confirm our hypothesis, human THP‑1 cells (1 × 106 cells/mL) were initially treated with 20 ng/mL phorbol 12‑myristate 13‑acetate (PMA) for 24 h. The PMA‑differentiated THP‑1 cells were treated with various levels of narirutin 2 h before lipopolysaccharide stimulation; after that, the cells were cultured for 24–48 h and then examined. The concentration of interferon‑gamma‑inducible protein‑10 (IP‑10) was measured using enzyme‑linked immunosorbent assay. Epigenetic regulation mechanisms were explored by chromatin immunoprecipitation assay. Results: Narirutin significantly suppressed IP‑10 production in M1 macrophage cells, and the suppressing effect was partly reversed by the estrogen receptor antagonist, the aryl‑hydrocarbon receptor antagonist, the peroxisome proliferator‑activated receptor (PPAR)‑α antagonist, and the PPAR‑γ antagonist. We also found that narirutin‑induced IP‑10 suppression can be modulated by both histone H3 and H4 acetylation. Conclusion: Our study suggests the potential of narirutin for the treatment of inflammatory disease by suppressing IP‑10.

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      Li, C., Wang, L., Kuo, C., Chen, Y., Tsai, M., & Hung, C. (2020). Narirutin Suppresses M1‑Related Chemokine InterferonGamma-Inducible Protein‑10 Production in Monocyte‑Derived M1 Cells via Epigenetic Regulation. Pharmacognosy Magazine, 16(71), 479–485. https://doi.org/10.4103/pm.pm_105_20