Salidroside inhibits MAPK, NF-κB, and STAT3 pathways in psoriasis-associated oxidative stress via SIRT1 activation

Fengli Xu,Jixiang Xu,Xia Xiong,Yongqiong Deng

doi:10.1080/13510002.2019.1658377

Fengli Xu, Jixiang Xu + Show 2 more

Open Access

https://doi.org/10.1080/13510002.2019.1658377

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Abstract

ABSTRACTObjectives: To unveil the role of SIRT1 in limiting oxidative stress in psoriasis and to further discuss the therapeutic prospects of salidroside in psoriasis.Methods: Literature from 2002 to 2019 was searched with “psoriasis”, “oxidative stress”, “SIRT1”, “salidroside” as the key words. Then, Oxidative stress in psoriasis and the role of SIRT1 were summarized and the potential role of salidroside in the disease was speculated.Results: Oxidative stress might contribute to the pathogenesis of psoriasis. High levels of ROS produced during oxidative stress lead to the release of inflammatory mediators, that, in turn, induce angiogenesis and excessive proliferation of keratinocytes. SIRT1 is a member of the sirtuin family, of which the activation lead to the inhibition of such oxidative stress signaling pathways MAPK, NF-κB, and STAT3, down-regulation of inflammatory factors, suppression of inflammation and keratinocyte hyperproliferation, and inhibition of angiogenesis. Salidroside, the main ingredient of Rhodiola, is known to exert antioxidant roles, which has been attributed to SIRT1 activation.Conclusion: Salidroside might inhibit oxidative stress singling pathways via SIRT1 activation, and could be as an ideal candidate for management of psoriasis.

Highlights

Psoriasis is a chronic inflammatory disease that affects 2%–5% of the world’s population
SIRT1 is a member of the sirtuin family, of which the activation lead to the inhibition of such oxidative stress signaling pathways MAPK, Nuclear factor-κB (NF-κB), and STAT3, down-regulation of inflammatory factors, suppression of inflammation and keratinocyte hyperproliferation, and inhibition of angiogenesis
It has been reported that the generation of oxidative stress could promote psoriasis through the MAPK, NF-κB, and STAT3 pathways and that it can be alleviated by inhibition of these three pathways [3,4]

Summary

Introduction

Psoriasis is a chronic inflammatory disease that affects 2%–5% of the world’s population. It is characterized by erythema, plaques, and scales, and is sometimes accompanied by itching [1]. The histological hallmarks of psoriasis include angiogenesis, abnormal keratinocyte proliferation, and infiltration of inflammatory cells. Some investigators have highlighted the genetic factors involved in the pathogenesis of psoriasis. TNF-α gene polymorphisms, including the SNP +489 allele, have been significantly associated with psoriatic arthritis susceptibility and severity [2]. Other previous studies have established their association with autoimmune diseases and environmental factors. It has been reported that the generation of oxidative stress could promote psoriasis through the MAPK, NF-κB, and STAT3 pathways and that it can be alleviated by inhibition of these three pathways [3,4]

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Conclusion