ArticleFrontiers in pharmacology2025
Polydatin ameliorates hyperhidrosis by targeting Aqp5 in a mouse model.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Microbial Fermentation Reduces Xerostomia-Related 5-Demethylnobiletin in Aurantii Fructus: A Chromatographic and Pharmacological Evaluation.Biomedical chromatography : BMC · 2026Article
- Don't Sweat It: Cannabinoid CB1 Receptors Reduce Sweating in a Mouse Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
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Authors and funding
6 authors.
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Abstract
Background: Primary focal hyperhidrosis (PFH) is a neurological dermatological disorder characterized by localized, excessive sweating. Current treatments have limitations, and postoperative compensatory hyperhidrosis remains a concern. Aquaporin 5 (AQP5) and neurologic factors such as Brain-Derived Neurotrophic Factor (BDNF) and Neuregulin-1 (NRG-1) are known to play key roles in sweat regulation. Polydatin, a natural compound with anti-inflammatory and neuroregulatory properties, has shown therapeutic potential in related conditions. Methods: This preclinical experimental study investigated the effects of Polydatin in a mouse model of hyperhidrosis. Mice were treated with different doses and durations of Polydatin. Aqp5 knockout mice were used to explore the AQP5-related pathway. Sweat gland function, gene and protein expression (AQP5, BDNF, NRG-1), and cell responses to acetylcholine stimulation were analyzed. Results: Polydatin at 50 mg/kg/day significantly reduced sweat secretion in hyperhidrotic mice (p < 0.001), while treatment duration showed no significant impact. The therapeutic effect was absent in Aqp5 knockout mice, confirming AQP5 dependence. Polydatin downregulated mRNA and protein expression of AQP5, Na Conclusion: Polydatin alleviates hyperhidrosis by targeting AQP5 and suppressing key neurologic factors, supporting its potential as a novel therapeutic approach for PFH.
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