1. Academic Validation
  2. Pseudoephedrine alleviates atopic dermatitis-like inflammatory responses in vivo and in vitro

Pseudoephedrine alleviates atopic dermatitis-like inflammatory responses in vivo and in vitro

  • Life Sci. 2020 Oct 1;258:118139. doi: 10.1016/j.lfs.2020.118139.
Xiaolei Chen 1 Jiacheng Lin 2 Qingsong Liang 3 Xiaoyin Chen 4 Zhongping Wu 5
Affiliations

Affiliations

  • 1 School of Basic Medicine Science, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai, China.
  • 2 School of Basic Medicine Science, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai, China; Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, 528 Zhangheng Road, Shanghai, China.
  • 3 Department of Dermatology, Bengbu Hospital of Traditional Chinese Medicine, 4339 Huaishangdadao Road, Bengbu, Anhui, China.
  • 4 College of Traditional Chinese Medicine, Jinan University, 601 Huangpu avenue Road, Guangzhou, Guangdong, China. Electronic address: tchenxiaoyin@jnu.edu.cn.
  • 5 School of Basic Medicine Science, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai, China. Electronic address: wzp@shutcm.edu.cn.
Abstract

Aims: Atopic dermatitis is a chronic inflammatory disease characterized by eczematous lesions and has become a serious health problem worldwide. Pseudoephedrine (PSE) is a nasal decongestant to treat the common cold. PSE has been reported that is beneficial to allergic diseases. However, whether PSE has the potential in atopic dermatitis remains to be elucidated.

Main methods: Male BALB/c mice were challenged with 2,4-dinitrochlorobenzene (DNCB) to induce atopic dermatitis-like lesion and orally administrated with PSE for two weeks. The skin hydration and the scratching behavior were detected. The skin lesions and histopathological changes were evaluated and inflammatory factors levels were detected. Human Keratinocytes (HaCaT cells) were stimulated by TNF-α/IFN-γ after PSE-pretreatment. The transcriptions of inflammatory factors were detected.

Key findings: PSE decreased skin lesion area and skin thickness in atopic dermatitis mice. PSE improved skin hydration and scratching. Histologically, PSE reduced mast cell and CD4+ cell infiltration. PSE suppressed serum TNF-α and IgE levels, reducing cytokines (IL-1β, IL-4, IL-6, IL-13, IL-33, TSLP, and IL-23) and neutrophil migration factors (CCL2 and MMP-9) in skin tissues. In addition, PSE inhibited TNF-α/IFN-γ-induced release of inflammatory factors (TNF-α, IL-1β, and IL-23) in HaCaT cells. Furthermore, PSE suppressed the activation of MAPKs and NF-κB signaling pathways in vivo and in vitro.

Significance: These results demonstrate that PSE could inhibit inflammatory responses in atopic dermatitis models. PSE may serve as a viable alternatives drug for the treatment of atopic dermatitis.

Keywords

Atopic dermatitis; DNCB; HaCaT; MAPKs; NF-κB; Pseudoephedrine.

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