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Capsiate Inhibits DNFB-Induced Atopic Dermatitis in NC/Nga Mice through Mast Cell and CD4+ T-Cell Inactivation.

Abstract
Capsaicin has many biological effects, such as antioxidant, anticancer, and antiangiogenic effects, but it is rarely used because of its high pungency. Capsiate, a nonpungent capsaicin analog, also has multiple biological effects, similar to those of capsaicin, but does not cause irritation. However, the effect of capsiate on allergic responses and immune cells has not been well studied. In this study, we investigated the effect of capsiate on atopic dermatitis, mouse CD4+ T cells, and mast cell activation. Capsiate inhibited DNFB-induced atopic dermatitis in NC/Nga mice. Topical treatment with capsiate suppressed serum IgE levels and cytokine and chemokine expression in the skin of DNFB-treated NC/Nga mice. In addition, it suppressed the activation of CD4+ T cells and mast cells, which are implicated in allergic diseases. Capsiate inhibited the differentiation of naïve CD4+ T cells into T helper type 1 (Th1), Th2, and Th17 cells. Treatment with capsiate inhibited the expression of pro-inflammatory cytokines and degranulation from activated bone marrow-derived mast cells through the inhibition of extracellular signal-regulated kinase signal pathways. Consistent with these results, treatment with capsiate inhibited passive cutaneous anaphylaxis. Taken together, our results suggest that capsiate might be a good candidate molecule for the treatment of allergic diseases such as atopic dermatitis.
AuthorsJi H Lee, Yun S Lee, Eun-Jung Lee, Ji H Lee, Tae-Yoon Kim
JournalThe Journal of investigative dermatology (J Invest Dermatol) Vol. 135 Issue 8 Pg. 1977-1985 (Aug 2015) ISSN: 1523-1747 [Electronic] United States
PMID25806854 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Dinitrofluorobenzene
  • capsiate
  • Capsaicin
Topics
  • Animals
  • CD4-Positive T-Lymphocytes (drug effects, pathology)
  • Capsaicin (analogs & derivatives, pharmacology, therapeutic use)
  • Cell Differentiation (drug effects)
  • Cell Proliferation (drug effects)
  • Dermatitis, Atopic (chemically induced, drug therapy, pathology)
  • Dinitrofluorobenzene (adverse effects)
  • Disease Models, Animal
  • MAP Kinase Signaling System (drug effects)
  • Mast Cells (drug effects, pathology)
  • Mice
  • Mice, Mutant Strains
  • Passive Cutaneous Anaphylaxis (drug effects)
  • Skin (drug effects, pathology)

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