Evaluation of Atractylodes macrocephala Koidz Extract as a Multi-Functional Natural Ingredient for Skin Barrier Repair
- 1Yunnan Characteristic Plant Extraction Laboratory, School of Chemical Science and Technology, Yunnan University, Kunming 650091, China
- 2Liwa Institute of Skin Health, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China
Abstract
Epidermal barrier damage triggers sensitive skin disorders. Synthetic skin repair agents frequently incur irritation, whereas medicinal and edible herbal ingredients offer milder alternatives. As a traditional Chinese medicinal herb, Atractylodes macrocephala Koidz remains inadequately characterized regarding its epidermal barrier repair efficacy. This work systematically characterized the barrier restoring capacity of A. macrocephala extract (AKE) via keratinocyte injured models, biochemical assays, spectroscopic interaction analysis, molecular docking and a tape stripping-induced mouse model of skin barrier impairment. AKE promoted keratinocyte migration, alleviated sodium lauryl sulfate triggered oxidative injury and enhanced ceramide synthesis. Moreover, AKE inhibited hyaluronidase, collagenase and elastase activities. Fluorescence quenching spectroscopy and thermodynamic analysis demonstrated spontaneous binding between AKE constituents and these skin degrading enzymes. At 50 μg/mL, AKE downregulated expression of pro-inflammatory cytokines interleukin (IL)-6 and IL-8 by suppressing the NF-κB inflammatory cascade, and restored occludin and keratin levels (p < 0.01 vs. the model group). It also exerted anti-Microsporum gypseum activity, with a minimum inhibitory concentration (MIC) of 92.36 ± 1.03 μg/mL, which alleviated inflammation and pruritus associated with dermatomycosis. In barrier-damaged mice, topical application of AKE recovered 81.2% of epidermal integrity (p < 0.001 vs. the model group) and normalized skin biomarkers. UHPLC-ESI-HRMS/MS combined with molecular docking identified atractylenolide I-II as potential bioactive compounds. In summary, AKE repairs damaged epidermis through multi-target modulation, indicating promising potential as a natural functional candidate for skin barrier repair.
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BibTeX
@article{liu2026evaluation,
title = {{Evaluation of Atractylodes macrocephala Koidz Extract as a Multi-Functional Natural Ingredient for Skin Barrier Repair}},
author = {Huan Liu and Le Yu and Chang-Yin Yang and Yu-Qiang Zhao and Lin Xu and Ying Zhou},
journal = {Molecules},
year = {2026},
month = oct,
doi = {10.3390/molecules31203713},
url = {https://www.mdpi.com/1420-3049/31/20/3713},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Evaluation of Atractylodes macrocephala Koidz Extract as a Multi-Functional Natural Ingredient for Skin Barrier Repair
AU - Huan Liu
AU - Le Yu
AU - Chang-Yin Yang
AU - Yu-Qiang Zhao
AU - Lin Xu
AU - Ying Zhou
PY - 2026
DA - 2026/10/01
JO - Molecules
DO - 10.3390/molecules31203713
UR - https://www.mdpi.com/1420-3049/31/20/3713
AB - Epidermal barrier damage triggers sensitive skin disorders. Synthetic skin repair agents frequently incur irritation, whereas medicinal and edible herbal ingredients offer milder alternatives. As a traditional Chinese medicinal herb, Atractylodes macrocephala Koidz remains inadequately characterized regarding its epidermal barrier repair efficacy. This work systematically characterized the barrier restoring capacity of A. macrocephala extract (AKE) via keratinocyte injured models, biochemical assays, spectroscopic interaction analysis, molecular docking and a tape stripping-induced mouse model of skin barrier impairment. AKE promoted keratinocyte migration, alleviated sodium lauryl sulfate triggered oxidative injury and enhanced ceramide synthesis. Moreover, AKE inhibited hyaluronidase, collagenase and elastase activities. Fluorescence quenching spectroscopy and thermodynamic analysis demonstrated spontaneous binding between AKE constituents and these skin degrading enzymes. At 50 μg/mL, AKE downregulated expression of pro-inflammatory cytokines interleukin (IL)-6 and IL-8 by suppressing the NF-κB inflammatory cascade, and restored occludin and keratin levels (p < 0.01 vs. the model group). It also exerted anti-Microsporum gypseum activity, with a minimum inhibitory concentration (MIC) of 92.36 ± 1.03 μg/mL, which alleviated inflammation and pruritus associated with dermatomycosis. In barrier-damaged mice, topical application of AKE recovered 81.2% of epidermal integrity (p < 0.001 vs. the model group) and normalized skin biomarkers. UHPLC-ESI-HRMS/MS combined with molecular docking identified atractylenolide I-II as potential bioactive compounds. In summary, AKE repairs damaged epidermis through multi-target modulation, indicating promising potential as a natural functional candidate for skin barrier repair.
SN - 1420-3049
ER -