Corydalis Tuber Extract Alleviates Atopic Dermatitis: Transcriptomics-Based Mechanism Prediction and In Vitro/In Vivo Studies

TL;DR

Corydalis Tuber extract reduces inflammation in atopic dermatitis by targeting immune pathways and reducing skin inflammation in mice.

Contribution

This study identifies specific compounds in Corydalis Tuber extract and their anti-inflammatory mechanisms in atopic dermatitis.

Findings

CTE reduced inflammatory markers like CCL17 and CCL22 in human skin cells.

Topical CTE improved dermatitis symptoms and reduced inflammation in a mouse model.

CTE inhibited immune pathways like JAK-STAT and NF-κB, lowering stress-related factors.

Abstract

Atopic dermatitis (AD) is a common inflammatory skin disease characterized by recurrent eczema and chronic itching, affecting a significant portion of the global population. This study investigated the effects of Corydalis Tuber 70% ethanol extract (CTE) on tumor necrosis factor-α- and interferon-γ (TI)-stimulated human keratinocytes (HaCaT) and a house dust mite-induced AD mouse model, elucidating its mechanism via transcriptome analysis. A total of 13 compounds, including columbamine, corydaline, dehydrocorydaline, and glaucine, were identified in CTE using ultra performance liquid chromatography-tandem mass spectrometry. CTE downregulated pathways related to cytokine signaling and chemokine receptors in TI-stimulated HaCaT cells. It significantly inhibited C-C motif chemokine ligand (CCL)5, CCL17, and CCL22 levels by blocking the Janus kinase-signal transducers and activators of transcription and nuclear factor kappa-light-chain-enhancer of activated B cells pathways. In the AD mouse model, topical CTE significantly decreased dermatitis scores, epidermal thickening, and inflammatory cell infiltration. Plasma levels of histamine, immunoglobulin E, CCL17, CCL22, corticosterone, and cortisol were reduced. Lesions showed decreased thymic stromal lymphopoietin, CD4+ T cells, interleukin-4, and intercellular adhesion molecule-1 expression. The findings demonstrate that CTE alleviates AD by modulating inflammatory mediators, cytokines, and chemokines, reducing inflammatory cell infiltration, and alleviating stress-related factors.

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