Background: Echinocystic acid (ECA), a pentacyclic triterpene enriched in various herbs, promotes anti-inflammatory and antioxidant activity; however, its therapeutic effects on atopic dermatitis (AD) or atopic march and the underlying mechanisms of action have not yet been fully elucidated.
Purpose: This study aimed to elucidate the effects and molecular mechanisms of ECA on AD and allergic inflammation.
Methods: We evaluated the inhibitory effects of ECA using a house dust mite (HDM)-induced AD mouse model and human keratinocytes.
Results: The results revealed that ECA improved AD symptoms by decreasing epidermal/dermal thickness, immune cell infiltration, and restoring skin barrier function, as well as an imbalanced immune response. In addition, repeated epicutaneous HDM challenges aggravated allergic inflammation in mice lungs, which was caused by the infiltration of immune cells and collagen deposition, whereas ECA alleviated these symptoms. Moreover, ECA suppressed the expression of T helper cell-derived cytokines, phosphorylation of extracellular signal-regulated kinase, and signal transducer and activator of transcription 1 in the skin and lungs of mice with HDM-induced AD, as well as inhibited the translocation of nuclear factor-κB in HaCaT keratinocytes.
Conclusion: This is the meaningful study to demonstrate that ECA improves allergic inflammation of the skin and lungs through recovery of the skin barrier, regulation of immune balance, and alleviation of lung inflammation, suggesting that ECA has therapeutic potential as an antiatopic and antiallergic agent that blocks the progression of AD to atopic march.
Keywords: Atopic dermatitis; Atopic march; Echinocystic acid; Immune balance; Lung inflammation; Skin barrier function.
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