Abstract

Aim Higenamine [1-[(4-hydroxyphenyl) methyl]-1, 2, 3, 4-tetrahydroisoquinoline-6, 7-diol], a potent cardiotonic compound from Aconitum, contributes to vascular relaxation and bronchodilation. However, the effects and mechanisms of action of higenamine on skin aging remain poorly understood. In this study, the effects of higenamine on UVB-induced photoaging were examined in the hairless mouse model. Methods The dorsal skin of hairless mice (CrlOri : SKH1) was exposed to chronic UVB irradiation (100–300 mJ/cm2 for 6 weeks), with subsequent administration of higenamine (1–20 mg/kg, p.o.) for 2 weeks. TGF-β, Smad3 DNA-binding phosphorylation, and COL1A1 levels were analyzed by immunohistochemistry, and histological analysis of the skin was performed via H&E and MT staining. Results Higenamine increased TGF-β, Smad3 DNA-binding phosphorylation, and COL1A1 expression in primary human fibroblast cells and mouse skin. Higenamine suppressed UVB-induced photoaging via skin recovery, improved epidermal thickness, and prevented Smad3, DNA-binding phosphorylation, and COL1A1 depletion via TGF-β signaling. Conclusion Higenamine enhances collagen production in the skin through TGF-β/Smad3 signaling and potentially suppresses UVB-induced skin aging.

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