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. 2020 Jun 11;10:9510. doi: 10.1038/s41598-020-66490-z

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Histological presentation of control skin, IMQ-induced psoriasiform dermatitis, and IMQ-induced psoriasiform dermatitis treated with ambrisentan or bosentan. (a,d) H&E staining of skin tissue harvested at day 6 (×400). Samples from the ear and back of control mice, IMQ-treated mice, and IMQ+ ambrisentan or bosentan-treated mice at day 6 (after treatment for five consecutive days with IMQ) were stained using H&E. (b,e) Epidermal thickness and inflammatory cell infiltration of control skin, IMQ-induced psoriasiform dermatitis, and IMQ-induced murine psoriasiform dermatitis treated with ambrisentan or bosentan. The epidermal thickness and number of dermal inflammatory cells were determined per high-power field from four mice per group. Data are presented as mean ± SEM. *P < 0.05, versus IMQ-treated group. (c,f) Immunohistochemical staining for ET-1 of samples from the ear and back of control mice, IMQ-treated mice, and IMQ+ ambrisentan or bosentan-treated mice (×400). Results are representative of similar results obtained in three independent experiments.