Inhibitory Effects of Urtica thunbergiana Ethanol Extract on Atopic Dermatitis-Induced NC/Nga Mice

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.

Liangxue-Qushi-Zhiyang Decoction Ameliorates DNCB-Induced Atopic Dermatitis in Mice through the MAPK Signaling Pathway Based on Network Pharmacology

“…Among them, the MAPK pathway, activated by EGF and EGFR signals, has been shown to control a wide range of physiological and pathological processes, including cell proliferation, gene expression, programmed cell death, and inflammation . Prior research has suggested that diminishing the expression of EGFR within the MAPK pathway can effectively alleviate the symptoms of AD in mice. , MAPKs, including ERK1/2 (MAPK3/1), JNK1/2/3, and p38 proteins (MAPK14), have been reported to be involved in AD. − IL-1β1, IL-6, and TNF-α act as proinflammatory cytokine genes, which can be activated by MAPK signaling pathways . Generally, an important cause of AD is the dysregulated Th1 and Th2 response .…”

Inhibitory Effects of Donkey Hide Gelatin on DNCB-Induced Atopic Dermatitis in NC/Nga Mice

“…We believe that DHG has potential for application as an anti-AD agent. TNF-α/IFN-γ induces keratinocyte inflammation via modulating different signaling pathways including the mitogen-activated protein kinases (MAPKs) and the nuclear factor-κB (NF-κB) pathways ( Ngo et al, 2020 ).…”

New Treatments for Atopic Dermatitis Targeting Skin Barrier Repair via the Regulation of FLG Expression

“…[ 209 ]. Another study found that Urtica thunbergiana, a Korean traditional medicine treatment, recovers the FLG and protects the AD skin by decreasing scratching and epidermal thickness, as well as by promoting SC hydration [ 210 ].…”