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

Isatidis folium or Isatis tinctoria 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-a (TNF-a) and interferon-? (IFN-?)-activated HaCaT cells. Oral administration of WIF reduced spleen weight, decreased serum IgE and TNF-a 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-a, IFN-?, 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-a/IFN-?-stimulated HaCaT cells. Overall, the results revealed that WIF ameliorated AD-like skin inflammation by suppressing proinflammatory cytokine and chemokine production via nuclear factor-?B pathway inhibition, suggesting WIF as a potential candidate for AD treatment.

Automated summary

This study aimed to evaluate the effects of Isatidis folium water extract (WIF) on atopic dermatitis (AD) and investigate the underlying mechanism. The results showed that oral administration of WIF reduced AD-like symptoms in mice and suppressed the production of proinflammatory cytokines and chemokines in HaCaT cells. These findings suggest that WIF may be a potential candidate for AD treatment by inhibiting the nuclear factor-κB pathway and reducing inflammation.