Abstract
Atopic dermatitis (AD) is a chronic, inflammatory skin disease that persists or repeatedly recurs in both childhood and adulthood. Urtica thunbergiana (UT) is an aroma herb with little-known pharmacological effects and anti-inflammatory activities against AD. This study investigated the immunomodulatory efficacy of 50% ethanol-extracted UT in necrosis factor-alpha/interferon-gamma (TNF-α/IFN-γ)-stimulated HaCaT cells in vitro and AD-Biostir-induced NC/Nga mice in vivo. The results showed that UT exhibits a dose-dependent increase in scavenged free radicals, reaching 76.0% ± 1.4% of scavenged 1,1-diphenyl-2-picrylhydrazyl at a concentration of 250 µg/mL. In addition, UT significantly downregulated the mRNA expression of the following pro-inflammatory cytokines and chemokines in TNF-α/IFN-γ-stimulated HaCaT cells: interleukin (IL)-6, IL-8, thymus- and activation-regulated chemokine, macrophage-derived chemokine, and regulated on activation normal T expressed and secreted. UT-treated HaCaT cells showed inhibition of the overexpression of chemokine-regulated signaling molecules, such as nuclear factor-kappa B, inhibitor of kappa B (IκBα), signal transducer and activator of transcription 1, and mitogen-activated protein kinases (MAPKs). UT dietary administration in AD-Biostir-induced NC/Nga mice treated and improved AD-like symptoms, such as scales, epidermal thickening, the dermatitis severity score, high trans-epidermal water loss, reduced skin hydration, increased mast cells, elevated serum immunoglobulin E levels, and an enlarged spleen. UT treatment inhibited the expression of phosphorylated forms of MAPKs, nuclear factor of activated T-cells 1, and regulator IκBα. It also upregulated filaggrin (FLG) production. Therefore, UT shows high anti-AD activity both in vitro and in vivo, and can be a useful anti-AD agent.
Highlights
Atopic dermatitis (AD) is a chronic, relapsing inflammatory disease of the skin, which is characterized by inflamed skin, pruritus, redness, and blisters with oozing and crusting through dry, rough skin
Intense pruritus leads to the behavior of scratching, which is an important symptom of AD associated with filaggrin (FLG)-regulated epidermis disruption [1]
We found that chlorogenic acid significantly enhanced the production of type I procollagen by regulating NFATc1 dephosphorylation
Summary
Atopic dermatitis (AD) is a chronic, relapsing inflammatory disease of the skin, which is characterized by inflamed skin, pruritus, redness, and blisters with oozing and crusting through dry, rough skin. AD onset is attributed to defective immune cells, including keratinocytes, monocytes, and Langerhans cells. These defective cells are hypersensitive to environmental agents, such as dust mites, food, weeds, and bacteria, leading to an overwhelming immune and inflammatory response. Antioxidants 2020, 9, 197 ligand 15 (RANTES/CCL5), and interleukins (ILs), are key mediators in the inflammatory response in skin diseases such as AD, subsequently upregulating the B-cell synthesis of immunoglobulin. Studies have shown that cell inflammatory signaling molecules, such as Janus kinase (JAK)/signal transducer, and activator of transcription (STAT), mitogen-activated protein kinases (MAPKs), and nuclear factor-kappa B (NF-κB), are involved in the development, immunity, cellular differentiation, and homeostasis of AD [3]
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