Abstract
The discovery of drugs for the treatment of allergic disease is an important subject in human health. The Artemisia iwayomogi (Compositae) (AIE) has been used as a traditional medicine in Korea and is known to have an anti-inflammatory effect. However, its specific mechanism of action is still unknown. In this report, we investigated the effect of AIE on the mast cell-mediated allergy model and studied the possible mechanism of action. AIE inhibited compound 48/80-induced systemic reactions and plasma histamine release in mice. AIE decreased immunoglobulin E (IgE)-mediated local allergic reaction, passive cutaneous anaphylaxis (PCA) reaction. AIE dose dependently attenuated histamine release from rat peritoneal mast cells activated by compound 48/80 or IgE. AIE decreased the compound 48/80-induced intracellular Ca2+. Furthermore, AIE decreased the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187-stimulated tumor necrosis factor-α and interleukin-6 gene expression and production in human mast cells. The inhibitory effect of AIE on the proinflammatory cytokine was p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) dependent. AIE attenuated PMA plus A23187-induced degradation of IκBα and nuclear translocation of NF-κB and specifically blocked activation of p38 MAPK but not that of c-jun N-terminal kinase and extracellular signal-regulated kinase. Our findings provide evidence that AIE inhibits mast cell-derived immediate-type allergic reactions and involvement of intracellular Ca2+, proinflammatory cytokines, p38 MAPK, and NF-κB in these effects.
| Original language | English |
|---|---|
| Pages (from-to) | 82-88 |
| Number of pages | 7 |
| Journal | Experimental Biology and Medicine |
| Volume | 230 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 2005 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Artemisia iwayomogi
- Interleukin-6
- Intracellular Ca
- Mast cells
- Nuclear factor-κB
- p38 mitogen-activated protein kinase
- Tumor necrosis factor-α
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