4.4 Article

Magnolol may contribute to barrier function improvement on imiquimod-induced psoriasis-like dermatitis animal model via the downregulation of interleukin-23

Journal

EXPERIMENTAL AND THERAPEUTIC MEDICINE
Volume 21, Issue 5, Pages -

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2021.9876

Keywords

interleukin-17; interleukin-23; psoriasis; magnolol; imiquimod; skin barrier

Funding

  1. Ministry of Science and Technology of Taiwan
  2. MOST107-2314-B-281-010-and [MOST-108-2314-B-281-002-]
  3. Cathay General Hospital [CGH-MR-A106024, CGH-MR-A109017]

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Magnolol, a polyphenolic compound, has been shown to have therapeutic effects in dermatological processes, but its application in psoriasis research is limited. The study demonstrated that downregulation of IL-23 by magnolol may contribute to improvement in barrier function in psoriatic skin models.
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-kappa B/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-gamma, and also significantly inhibited the protein expression of interleukin (IL)-23, IL-1 beta, IL-6, tumor necrosis factor-alpha and interferon-gamma. 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.

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