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Peer-reviewedCC BY-NCAnnals of dermatology

Amygdalin Targets PLAU to Modulate Immune-Inflammatory Signaling and Ameliorate Atopic Dermatitis: Evidence From Multi-Omics and an Animal Model.

  • Jiayin Zhang1
  • Mi Zhong2
  • Fen Zeng2
  1. 1Department of Dermatology, Affiliated Hospital of Jiangnan University, Wuxi, China. [email protected].
  2. 2Department of Dermatology, Affiliated Hospital of Jiangnan University, Wuxi, China.
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Abstract

Background

Atopic dermatitis (AD) is a chronic inflammatory skin disorder with limited therapeutic options.Objective

This study evaluated the therapeutic potential of amygdalin by identifying urokinase-type plasminogen activator (uPA/PLAU)-associated molecular targets and immune-inflammatory signaling pathways, aiming to explore a potential strategy for natural product-based interventions.Methods

Transcriptomics, network pharmacology, and molecular docking were integrated to predict potential targets of amygdalin and intersect them with AD-related differentially expressed genes to identify key candidate molecules. A 2,4-dinitrochlorobenzene-induced BALB/c mouse model was used to evaluate therapeutic effects through histopathology, cytokine profiling, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot analyses of PLAU/uPA-associated signaling, including the NLR family pyrin domain containing 3 (NLRP3) inflammasome and Toll-like receptor 4 (TLR4)/MyD88/nuclear factor (NF)-κB pathways.Results

PLAU was identified as a key candidate target potentially involved in the action of amygdalin. In vivo, amygdalin significantly reduced dermatitis severity and ear thickness (p<0.001), improved histopathology, and lowered serum immunoglobulin E, histamine, and thymus- and activation-regulated chemokine as well as skin interleukin (IL)-6, IL-1β, and tumor necrosis factor-α levels (p<0.001). It also partially corrected Th1/Th2 imbalance by increasing interferon-γ and decreasing IL-4 and IL-13 (p<0.001). qRT-PCR and Western blot showed reduced expression of PLAU/uPA, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and cathepsin K, together with reduced activation of the NLRP3 inflammasome and TLR4/MyD88/NF-κB signaling.Conclusion

Amygdalin exhibited anti-inflammatory and immunoregulatory effects in experimental AD and was associated with modulation of PLAU/uPA-related immune-inflammatory pathways, suggesting potential as a multi-target natural therapeutic candidate. However, the present study did not directly quantify or fully characterize the cyanogenic risk of amygdalin, and its safety profile-particularly regarding cyanide generation-requires further evaluation in dedicated toxicological investigations.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026amygdalin,
  title = {{Amygdalin Targets PLAU to Modulate Immune-Inflammatory Signaling and Ameliorate Atopic Dermatitis: Evidence From Multi-Omics and an Animal Model.}},
  author = {Jiayin Zhang and Mi Zhong and Fen Zeng},
  journal = {Annals of dermatology},
  year = {2026},
  month = oct,
  doi = {10.5021/ad.25.201},
  url = {https://europepmc.org/article/MED/42845201},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Amygdalin Targets PLAU to Modulate Immune-Inflammatory Signaling and Ameliorate Atopic Dermatitis: Evidence From Multi-Omics and an Animal Model.
AU  - Jiayin Zhang
AU  - Mi Zhong
AU  - Fen Zeng
PY  - 2026
DA  - 2026/10/01
JO  - Annals of dermatology
DO  - 10.5021/ad.25.201
UR  - https://europepmc.org/article/MED/42845201
AB  - Background  Atopic dermatitis (AD) is a chronic inflammatory skin disorder with limited therapeutic options.Objective  This study evaluated the therapeutic potential of amygdalin by identifying urokinase-type plasminogen activator (uPA/PLAU)-associated molecular targets and immune-inflammatory signaling pathways, aiming to explore a potential strategy for natural product-based interventions.Methods  Transcriptomics, network pharmacology, and molecular docking were integrated to predict potential targets of amygdalin and intersect them with AD-related differentially expressed genes to identify key candidate molecules. A 2,4-dinitrochlorobenzene-induced BALB/c mouse model was used to evaluate therapeutic effects through histopathology, cytokine profiling, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot analyses of PLAU/uPA-associated signaling, including the NLR family pyrin domain containing 3 (NLRP3) inflammasome and Toll-like receptor 4 (TLR4)/MyD88/nuclear factor (NF)-κB pathways.Results  PLAU was identified as a key candidate target potentially involved in the action of amygdalin. In vivo, amygdalin significantly reduced dermatitis severity and ear thickness (p<0.001), improved histopathology, and lowered serum immunoglobulin E, histamine, and thymus- and activation-regulated chemokine as well as skin interleukin (IL)-6, IL-1β, and tumor necrosis factor-α levels (p<0.001). It also partially corrected Th1/Th2 imbalance by increasing interferon-γ and decreasing IL-4 and IL-13 (p<0.001). qRT-PCR and Western blot showed reduced expression of PLAU/uPA, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and cathepsin K, together with reduced activation of the NLRP3 inflammasome and TLR4/MyD88/NF-κB signaling.Conclusion  Amygdalin exhibited anti-inflammatory and immunoregulatory effects in experimental AD and was associated with modulation of PLAU/uPA-related immune-inflammatory pathways, suggesting potential as a multi-target natural therapeutic candidate. However, the present study did not directly quantify or fully characterize the cyanogenic risk of amygdalin, and its safety profile-particularly regarding cyanide generation-requires further evaluation in dedicated toxicological investigations.
SN  - 1013-9087
SN  - 2005-3894
ER  -