Resveratrol and Its Derivatives in Inflammatory Skin Disorders-Atopic Dermatitis and Psoriasis: A Review

Abstract

Atopic dermatitis (AD) and psoriasis are inflammatory skin diseases whose prevalence has increased worldwide in recent decades. These disorders contribute to patients' decreased quality of life (QoL) and constitute a socioeconomic burden. New therapeutic options for AD and psoriasis based on natural compounds are being investigated. These include resveratrol (3,5,40-trihydroxystilbene) and its derivatives, which are produced by many plant species, including grapevines. Resveratrol has gained interest since the term "French Paradox", which refers to improved cardiovascular outcomes despite a high-fat diet in the French population, was introduced. Resveratrol and its derivatives have demonstrated various health benefits. In addition to anti-cancer, anti-aging, and antibacterial effects, there are also anti-inflammatory and antioxidant effects that can affect the molecular pathways of inflammatory skin disorders. A comprehensive understanding of these mechanisms may help develop new therapies. Numerous in vivo and in vitro studies have been conducted on the therapeutic properties of natural compounds. However, regarding resveratrol and its derivatives in treating AD and psoriasis, there are still many unexplained mechanisms and a need for clinical trials. Considering this, in this review, we discuss and summarize the most critical research on resveratrol and its derivatives in animal and cell models mimicking AD and psoriasis.

Keywords: atopic dermatitis; derivatives; inflammatory skin disorders; psoriasis; resveratrol.

Figure 1

The relationships between resveratrol’s anti-inflammatory and antioxidant effects and its derivatives in developing inflammatory skin disorders. Resveratrol may affect inflammation through its antioxidant activity and scavenging of free radicals. Key inflammation suppressors are ROS because they trigger the apoptosis of neutrophils. There is a connection between oxidative stress and the proper functioning of the skin. The phenomenon of oxidative stress, an increase in the level of free radicals or their imbalance, can lead to the degradation of cellular proteins, lipid oxidation, cell apoptosis, tissue damage, altered T helper cell response, secretion of IL-17, and changes in DNA, which, in turn, can lead to skin disorders. IL-1β: interleukin 1β; IL-6: interleukin 6; IL-8: interleukin 8; IL-23p19: interleukin 23p19; TNF-α: tumor necrosis factor α; MCP-1: monocyte chemoattractant protein 1; IFN-γ: interferon-γ; NFκB: nuclear factor kappa B; COX-1: cyclooxygenase-1; COX-2: cyclooxygenase-2; PGE2: prostaglandin E2; IgE: immunoglobulin E; AQP-3: aquaporin 3; NO: nitric oxide; ROS: reactive oxygen species; IL-17: interleukin-17.

Figure 2

The relationships and molecular pathways of resveratrol and its derivatives reported in studies on AD-like and psoriasis-like cell models. (A) Changes observed after using resveratrol and its derivatives in a cellular model mimicking AD; (B) changes observed after using resveratrol and its derivatives in a cellular model mimicking psoriasis. AD: atopic dermatitis; HDMs: house dust mites; HMGB1: high-mobility group box 1 protein; RAGE: receptors for advanced glycation end products; pNF-κB: phosphorylated nuclear factor-κB; p-PI3K: phosphoinositide 3-kinase; p-ERK1/2: phosphorylated extracellular signal-regulated kinase; IL-2Rα: interleukin-2 receptor α; IL-4: interleukin 4; IL-17α: interleukin 17 α; IL-31: interleukin 31; IL-25: interleukin 25; IL-33: interleukin 33; TSLP: thymic stromal lymphopoietin; IL-17A: interleukin 17A, IL-19: interleukin 19.

Figure 3

The relationships and molecular pathways of resveratrol and its derivatives reported in studies on AD-like and psoriasis-like animal models. (A) Changes observed after using resveratrol and its derivatives in a mouse model mimicking AD; (B) changes observed after using resveratrol and its derivatives in a cellular model mimicking AD; (C) changes observed after using resveratrol and its derivatives in a mouse model mimicking psoriasis; (D) changes observed after using resveratrol and its derivatives in a cellular model mimicking psoriasis. HaCaT: human keratinocyte cell line; TEWL: transepidermal water loss; CXCL8: interleukin 8.

Figure 4

The relationships and molecular pathways of resveratrol and its derivatives reported in studies on AD-like and psoriasis-like cell models. (A) Changes observed after using resveratrol and its derivatives in a cellular model mimicking AD; (B) changes observed after using resveratrol and its derivatives in a cellular model mimicking psoriasis. NHEKs: normal human epidermal keratinocytes; HMC-1: human mast cell line; MMP-1: matrix metalloproteinase 1; MMP-9: matrix metalloproteinase 9; IκBα: NF-kappaB inhibitor alpha; RIP2: receptor-interacting protein-2 kinase; p62: protein p62; Sirt1: sirtulin 1, Akt: protein kinase B (PKB).