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'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation
Psoriasis is an immune-mediated dermatosis characterized by T-lymphocyte-mediated epidermal hyperplasia, for which there are currently no effective clinical treatments. 'Psoriasis 1' is a Chinese herbal medicine formulation that has been recently used extensively in China for treating pati...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7447312/ https://www.ncbi.nlm.nih.gov/pubmed/32945358 http://dx.doi.org/10.3892/ijmm.2020.4695 |
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author | Gao, Yang Sun, Wen Cha, Xushan Wang, Hailong |
author_facet | Gao, Yang Sun, Wen Cha, Xushan Wang, Hailong |
author_sort | Gao, Yang |
collection | PubMed |
description | Psoriasis is an immune-mediated dermatosis characterized by T-lymphocyte-mediated epidermal hyperplasia, for which there are currently no effective clinical treatments. 'Psoriasis 1' is a Chinese herbal medicine formulation that has been recently used extensively in China for treating patients with psoriasis. However, the molecular mechanism of action of this potent formulation has not yet been fully elucidated. In the present study, the effects of 'Psoriasis 1' on T ymphocytes in patients with psoriasis were investigated and the underlying molecular mechanism was discussed. Blood samples were collected from 40 patients with psoriasis. ELISA was employed to assess the levels of tumour necrosis factor-α, interferon-γ, interleukin (IL)-2, IL-6, transforming growth factor-β, IL-4, IL-12, IL-23 and vitamin D (VD). Western blot and quantitative PCR analyses were used to investigate the expression levels of VD receptor (VDR) and signal transducer and activator of transcription (STAT)4 in T lymphocytes. 'Psoriasis 1' was observed to significantly increase CD4(+) T cells. It also notably upregulated the mRNA and protein expression of VDR, and downregulated the mRNA and protein expression of STAT4. Moreover, the suppression of VDR was found to aggravate the inflammatory response, which was reversed by 'Psoriasis 1.' Thus, this formulation reportedly decreased the inflammation mediated by T lymphocytes in patients with psoriasis through inhibiting VDR-mediated STAT4 inactivation. |
format | Online Article Text |
id | pubmed-7447312 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-74473122020-08-28 'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation Gao, Yang Sun, Wen Cha, Xushan Wang, Hailong Int J Mol Med Articles Psoriasis is an immune-mediated dermatosis characterized by T-lymphocyte-mediated epidermal hyperplasia, for which there are currently no effective clinical treatments. 'Psoriasis 1' is a Chinese herbal medicine formulation that has been recently used extensively in China for treating patients with psoriasis. However, the molecular mechanism of action of this potent formulation has not yet been fully elucidated. In the present study, the effects of 'Psoriasis 1' on T ymphocytes in patients with psoriasis were investigated and the underlying molecular mechanism was discussed. Blood samples were collected from 40 patients with psoriasis. ELISA was employed to assess the levels of tumour necrosis factor-α, interferon-γ, interleukin (IL)-2, IL-6, transforming growth factor-β, IL-4, IL-12, IL-23 and vitamin D (VD). Western blot and quantitative PCR analyses were used to investigate the expression levels of VD receptor (VDR) and signal transducer and activator of transcription (STAT)4 in T lymphocytes. 'Psoriasis 1' was observed to significantly increase CD4(+) T cells. It also notably upregulated the mRNA and protein expression of VDR, and downregulated the mRNA and protein expression of STAT4. Moreover, the suppression of VDR was found to aggravate the inflammatory response, which was reversed by 'Psoriasis 1.' Thus, this formulation reportedly decreased the inflammation mediated by T lymphocytes in patients with psoriasis through inhibiting VDR-mediated STAT4 inactivation. D.A. Spandidos 2020-10 2020-08-06 /pmc/articles/PMC7447312/ /pubmed/32945358 http://dx.doi.org/10.3892/ijmm.2020.4695 Text en Copyright: © Gao et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Gao, Yang Sun, Wen Cha, Xushan Wang, Hailong 'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation |
title | 'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation |
title_full | 'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation |
title_fullStr | 'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation |
title_full_unstemmed | 'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation |
title_short | 'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation |
title_sort | 'psoriasis 1' reduces t-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin d receptor-mediated stat4 inactivation |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7447312/ https://www.ncbi.nlm.nih.gov/pubmed/32945358 http://dx.doi.org/10.3892/ijmm.2020.4695 |
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