‘Psoriasis 1’ reduces T‑lymphocyte‑mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor‑mediated STAT4 inactivation
- Yang Gao
- Wen Sun
- Xushan Cha
- Hailong Wang
Affiliations: Division of Rheumatology, Guang An Men Hospital, China Academy of Chinese Medical Science, Beijing 100053, P.R. China, Department of Dermatology, The First People's Hospital of Jingmen, Jingmen, Hubei 448000, P.R. China, Department of Dermatology, The First Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangzhou, Guangdong 510000, P.R. China
- Published online on: August 6, 2020 https://doi.org/10.3892/ijmm.2020.4695
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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.