Selenium-Rich Yeast Peptide Fraction Ameliorates Imiquimod-Induced Psoriasis-like Dermatitis in Mice by Inhibiting Inflammation via MAPK and NF-κB Signaling Pathways.

Hengke Guo,Hongmei Liu,Min Li

doi:10.3390/ijms23042112

Abstract

Psoriasis, a chronic and immune-mediated inflammatory disease, adversely affects patients’ lives. We previously prepared selenium-rich yeast peptide fraction (SeP) from selenium-rich yeast protein hydrolysate and found that SeP could effectively alleviate ultraviolet radiation-induced skin damage in mice and inhibited H2O2-induced cytotoxicity in cultured human epidermal keratinocyte (HaCaT) cells. This study aimed to investigate whether SeP had a protective effect on imiquimod (IMQ)-induced psoriasis-like dermatitis in mice and the underlying mechanisms. Results showed that SeP significantly ameliorated the severity of skin lesion in IMQ-induced psoriasis-like mouse model. Moreover, SeP treatment significantly attenuated the expression of key inflammatory cytokines, including interleukin (IL)-23, IL-17A, and IL-17F, in the dorsal skin of mice. Mechanistically, SeP application not only inhibited the activation of JNK and p38 MAPK, but also the translocation of NF-κB into the nucleus in the dorsal skin. Furthermore, SeP treatment inhibited the levels of inflammatory cytokines and the activation of MAPK and NF-κB signaling induced by lipopolysaccharide in HaCaT cells and macrophage cell line RAW264.7. Overall, our findings showed that SeP alleviated psoriasis-like skin inflammation by inhibiting MAPK and NF-κB signaling pathways, which suggested that SeP would have a potential therapeutic effect against psoriasis.

Highlights

Psoriasis, a chronic immune-mediated inflammatory skin disease, affects over 60 million people worldwide [1,2]
Our findings showed that selenium-rich yeast peptide fraction (SeP) alleviated psoriasislike skin inflammation by inhibiting mitogen-activated protein kinases (MAPK) and nuclear factor-κB (NF-κB) signaling pathways, which suggested that
The anti-psoriatic effect of SeP was evaluated by using IMQ-induced psoriasis-like dermatitis mouse model

Summary

Introduction

A chronic immune-mediated inflammatory skin disease, affects over 60 million people worldwide [1,2]. Psoriasis was recognized by World Health Organization (WHO) as a “chronic, non-communicable, painful, disfiguring, and disabling disease for which there is no cure” in 2014 [2]. Inflammatory cytokines, produced by activated leucocytes, alter growth and differentiation of resident skin cells, especially keratinocytes [3]. Clinical and genetic studies focusing on the immune systems have highlighted the pivotal roles of inflammatory cytokines, such as interleukin (IL)-17, IL-23, and tumor-necrosis factor-α (TNF-α), and two fundamentally different cell types, including epidermal keratinocytes and mononuclear leukocytes, in the pathogenesis of psoriasis [1,4,5]. Nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPK) are the important potential molecular pathways involved in the pathogenesis of psoriasis through upregulating the pro-inflammatory cytokines and chemokines expression [4]. Psoriasis cannot be cured currently, and new therapies based on its pathogenesis are needed

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