Magnolol may contribute to barrier function improvement on imiquimod‑induced psoriasis‑like dermatitis animal model via the downregulation of interleukin‑23
- Jiun-Wen Guo
- Yu-Pin Cheng
- Chih-Yi Liu
- Haw-Yueh Thong
- Yang Lo
- Chen-Yu Wu
- Shiou-Hwa Jee
Affiliations: Department of Medical Research, Cathay General Hospital, Taipei 10630, Taiwan, R.O.C., Department of Dermatology, Cathay General Hospital, Taipei 10630, Taiwan, R.O.C., Division of Pathology, Sijhih Cathay General Hospital, New Taipei City 22174, Taiwan, R.O.C., Department of Dermatology, Shin‑Kong Wu Ho‑Su Memorial Hospital, Taipei 11101, Taiwan, R.O.C.
- Published online on: March 1, 2021 https://doi.org/10.3892/etm.2021.9876
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Psoriasis is a chronic, recurrent, immune‑mediated disease involving the skin and joints. Epidermal hyperproliferation, abnormal keratinocyte differentiation, angiogenesis with blood vessel dilatation, and excess T helper type‑1 (Th‑1) and Th‑17 cell infiltration are the main histopathological features of psoriasis. Magnolol is a polyphenolic compound that exerts its biological properties through a variety of mechanisms such as the NF‑κB/MAPK, Nrf2/HO‑1 and PI3K/Akt pathways. Magnolol has been demonstrated to exert a number of therapeutic effects on dermatological processes, including acting as an anti‑inflammation, antiproliferation and antioxidation agent. However, few studies have been published on the effect of magnolol on psoriasis. Therefore, the present study aimed to elucidate the mechanism of action of magnolol on psoriasis. BALB/c mice were treated topically with imiquimod (IMQ) to induce psoriasis‑like dermatitis, and were randomly assigned to the control, vehicle control, low‑ and high‑dose magnolol, and 0.25% desoximetasone ointment treatment groups in order to investigate skin barrier function, any changes in the levels of cytokines and for the histological assessment. High doses of magnolol were indicated to be able to improve the barrier function following IMQ‑induced barrier disruption. Magnolol activated peroxisome proliferator‑activated receptor‑γ, and also significantly inhibited the protein expression of interleukin (IL)‑23, IL‑1β, IL‑6, tumor necrosis factor‑α and interferon‑γ. However, administering a high dose of magnolol did not lead to any improvement in the clinical and pathological features of the psoriasis severity Taken together, these results demonstrated that downregulation of IL‑23 may contribute to barrier function improvement in a psoriatic skin model.