# The therapeutic potential of Astragalus membranaceus in atopic dermatitis: from traditional applications and modern pharmacological research to regulation of the Gut-Skin Axis

**Authors:** Chengshuang Lu, Yuping Zeng, Guo Wang, Buqing Lou, Yifan Wang, Wancheng Liu, Zhiming Yan, Haoyang Fu

PMC · DOI: 10.3389/fphar.2025.1685708 · Frontiers in Pharmacology · 2025-11-07

## TL;DR

Astragalus membranaceus may help treat atopic dermatitis by reducing gut-skin inflammation, offering a safer alternative to current treatments.

## Contribution

This study proposes a novel mechanism for Astragalus membranaceus in AD via the Gut-Skin Axis, supported by network pharmacology and molecular simulations.

## Key findings

- Astragalus membranaceus may inhibit gut-derived inflammation linked to atopic dermatitis.
- 89 common targets were identified between Astragalus membranaceus and atopic dermatitis.
- Key signaling pathways like IL-6, TNF-α, NF-κB, and IL-17 are implicated in AD progression.

## Abstract

Atopic dermatitis (AD) is a difficult-to-treat and recurrent skin condition that often imposes a heavy burden on patients and healthcare systems due to the high costs associated with its treatment and management. Astragalus membranaceus (AM), as a botanical drug, has been shown to alleviate skin diseases through multiple mechanisms. However, its systematic mechanism of action against AD remains unclear. This research summarizes the molecular mechanisms through which AM and its active components (polysaccharides, saponins, flavonoids) mitigate AD. The study proposes, for the first time, that AM may alleviate the onset and progression of AD by inhibiting the translocation of gut-derived inflammatory factors to the skin through the Gut-Skin Axis (GSA). Through comprehensive analysis of network pharmacology, molecular docking, and molecular dynamics simulations, compounds with potentially high activity of AM were preliminarily screened. The potential interaction mechanism between this compound molecule and the target protein in AD treatment was further explored. A total of 89 common targets were identified between AM and AD. Enrichment analysis suggests that signaling pathways such as IL-6, TNF-α, NF-κB, and IL-17 may serve as key regulatory hubs in the progression of AD. At conventional doses, AM exhibits a good safety profile. However, the risk of interactions when combined with traditional AD treatments (such as tacrolimus) warrants attention, necessitating enhanced safety evaluations before clinical application. Overall, AM holds potential as an adjunctive therapy for mitigating side effects and improving symptoms, offering a safer alternative to existing treatments. It contributes to shifting AD treatment strategies from purely symptom control toward addressing both symptoms and underlying causes.

## Linked entities

- **Chemicals:** saponins (PubChem CID 6540709), tacrolimus (PubChem CID 445643)
- **Diseases:** atopic dermatitis (MONDO:0004980)

## Full-text entities

- **Genes:** IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}
- **Diseases:** inflammatory (MESH:D007249), skin condition (MESH:D012871), AD (MESH:D003876)
- **Chemicals:** tacrolimus (MESH:D016559), polysaccharides (MESH:D011134), flavonoids (MESH:D005419), saponins (MESH:D012503)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12634398/full.md

## References

225 references — full list in the complete paper: https://tomesphere.com/paper/PMC12634398/full.md

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Source: https://tomesphere.com/paper/PMC12634398