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Gomisin M2 ameliorates imiquimod‐induced psoriasis‐like skin inflammation via the inhibition of mitogen‐activated protein kinase
Author(s) -
Kim Namkyung,
Kang Jinjoo,
Kim Hyemi,
Kim SangHyun
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.lb47
Subject(s) - hacat , psoriasis , tumor necrosis factor alpha , inflammation , imiquimod , medicine , chemokine , immunology , proinflammatory cytokine , pharmacology , interleukin , cytokine , chemistry , in vitro , biochemistry
Psoriasis (PS) is a chronic inflammatory skin disease with complex pathogenesis. Gomisin M2 (GM2) is a natural product extracted from Schisandra chinensis (Turcz.) Baill. In this study, we aimed to investigate the pharmacological effects of GM2 on PS‐like skin inflammation. For induction of PS‐like skin inflammation, imiquimod (IMQ) cream topically applied to the back skin of female C57BL/6J mice for 7 consecutive days. Oral administration of GM2 (0.1, 1 or 10 mg/kg) reduced the symptoms of PS‐like skin inflammation based on Psoriasis Area and Severity Index and histological observation. GM2 reduced serum levels of tumor necrosis factor (TNF)‐α, IgG2a, and myeloperoxidase. It also decreased MPO‐associated cell infiltration in skin tissue in a dose‐dependent manner. Furthermore, GM2 decreased production of Th1 and Th17‐related cytokines such as TNF‐α, interferon (IFN)‐γ, interleukin (IL)‐8, IL‐1β and IL‐17A in the back skin. For in vitro, we investigated the pharmacological effects of GM2 on TNF‐α and IFN‐γ stimulated keratinocytes (HaCaT). Pre‐treatment of GM2 (0.1, 1, or 10 μM) alleviated PS‐associated cytokines such as TNF‐α, IL‐1β, IL‐6, IL‐8, and Chemokine (C‐C motif) ligand 17. GM2 inhibited phosphorylation to mitogen‐activated protein kinase in the activated HaCaT. Our study reveals that GM2 possesses anti‐inflammatory effect on PS. Based on our results, we propose that GM2 could be a potential therapeutic candidate on PS. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .