Anti-Atopic Effect of Isatidis Folium Water Extract in TNF-α/IFN-γ-Induced HaCaT Cells and DNCB-Induced Atopic Dermatitis Mouse Model

• Published in: Molecules (Basel, Switzerland) Switzerland), 2023-05, Vol.28 (9), p.3960
• Main Authors: Min, Ga-Yul, Kim, Tae In, Kim, Ji-Hye, Cho, Won-Kyung, Yang, Ju-Hye, Ma, Jin Yeul
• Format: Article
• Language: English
• Subjects: Advertising executives; Allergens; Allergies; Analysis; Animals; anti-inflammation; Atopic dermatitis; Biological response modifiers; Biomarkers; CCL17 protein; CCL20 protein; CCL22 protein; Cell activation; Chemokines; Chemokines - metabolism; Cytokines; Cytokines - metabolism; Cytoplasm; Dermatitis; Dermatitis, Atopic - chemically induced; Dermatitis, Atopic - drug therapy; Dermatitis, Atopic - metabolism; Dermis; Dinitrochlorobenzene - adverse effects; Dinitrochlorobenzene - metabolism; Eczema; Edema; Erythema; Extracellular signal-regulated kinase; Flowering; Gene expression; HaCaT Cells; Herbal medicine; Humans; Immunoglobulin E; Inflammation; Interferon; Interferon-gamma - metabolism; Interleukin 13; Isatidis folium; Isatis tinctoria L; Keratinocytes; Kinases; Leukocytes (eosinophilic); Lymphocytes; Lymphocytes T; MAP kinase; Medicinal plants; Mice; Monocyte chemoattractant protein 1; NF-kappa B - metabolism; Oral administration; Protein expression; Protein kinases; Protein transport; Proteins; Quality of life; RANTES; RNA; RNA, Messenger - genetics; Skin; Skin diseases; Spleen; Steroids; T cells; Thymus; Translocation; Tumor necrosis factor; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Water - metabolism; Weight reduction; γ-Interferon
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules28093960

Isatidis folium or L. is a flowering plant of the Brassicaceae family, commonly known as woad, with an ancient and well-documented history as an indigo dye and medicinal plant. This study aimed to evaluate the anti-atopic dermatitis (AD) effects of Isatidis folium water extract (WIF) using a 2,4-dinitrochlorobenzene (DNCB)-induced AD-like mouse model and to investigate the underlying mechanism using tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ)-activated HaCaT cells. Oral administration of WIF reduced spleen weight, decreased serum IgE and TNF-α levels, reduced epidermal and dermal thickness, and inhibited eosinophil and mast cell recruitment to the dermis compared to DNCB-induced control groups. Furthermore, oral WIF administration suppressed extracellular signal-regulated kinase and p38 mitogen-activated protein kinase protein expression levels, p65 translocation from the cytoplasm to the nucleus, and mRNA expression of TNF-α, IFN-γ, interleukin (IL)-6, and IL-13 in skin lesion tissues. In HaCaT cells, WIF suppressed the production of regulated upon activation, normal T cell expressed and secreted (RANTES), thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC), MCP-1, and MIP-3a, which are inflammatory cytokines and chemokines related to AD, and inhibited the mRNA expression of RANTES, TARC, and MDC in TNF-α/IFN-γ-stimulated HaCaT cells. Overall, the results revealed that WIF ameliorated AD-like skin inflammation by suppressing proinflammatory cytokine and chemokine production via nuclear factor-κB pathway inhibition, suggesting WIF as a potential candidate for AD treatment.