Isochlorogenic acid A ameliorates atopic dermatitis by modulating JAK/STAT3, NF-κB, and MAPK pathways in a DNFB/PM2.5-induced mouse model.

Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by intense itching, eczematous lesions, and impaired skin barrier function. AD causes severe itching and inflammation, which significantly reduces the patient's quality of life. Various treatments are being developed to treat AD, but their use is limited due to some side effects. This study investigates the therapeutic potential of isochlorogenic acid A (ICA), a polyphenolic compound with anti-inflammatory and antioxidant properties, in a murine model of DNFB/PM2.5-induced AD. ICA significantly reduced dermatitis scores, skin swelling, and scratching behavior, indicating alleviation of inflammation and pruritus. Histological analysis revealed that ICA decreased epidermal hyperplasia and mast cell infiltration, while immunohistochemical staining showed increased expression of filaggrin and involucrin, key proteins for skin barrier integrity. ICA also reduced levels of pro-inflammatory cytokines IL-4 and IL-31 and attenuated oxidative stress by enhancing antioxidant enzyme activity. Mechanistically, ICA inhibited the JAK/STAT3, NF-κB, and MAPK signaling pathways, which are central to AD pathogenesis. These findings demonstrate that ICA ameliorates AD by modulating inflammatory and oxidative stress pathways, restoring skin barrier function, and suppressing cytokine production. ICA represents a promising natural therapeutic agent for AD, with potential applications in clinical settings.