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ORIGINAL ARTICLE
Year : 2020  |  Volume : 16  |  Issue : 71  |  Page : 479-485

Narirutin suppresses M1-related chemokine interferon-gamma-inducible protein-10 production in monocyte-derived M1 cells via epigenetic regulation


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

Correspondence Address:
Chih-Hsing Hung
Department of Pediatrics, Kaohsiung Municipal Siaoqang Hospital, No. 482, Shanming Road, Siaogang District, Kaohsiung City 812
Republic of China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_105_20

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Background: Flavonoids are groups of natural phytonutrients found in fruits and vegetables that have recently become popular because of their anti-oxidation and anti-inflammatory ability. Narirutin is a flavanone which has been proven to have anti-inflammation effects, although its fundamental mechanisms are not understood. 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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