Polydatin ameliorates hyperhidrosis by targeting Aqp5 in a mouse model.

Area of Science:

• Dermatology
• Neurology
• Pharmacology

Background:

• Primary focal hyperhidrosis (PFH) is a neurological dermatological condition causing excessive localized sweating.
• Current treatments for PFH have limitations, and postoperative compensatory hyperhidrosis is a significant concern.
• Aquaporin 5 (AQP5) and neuroregulatory factors like Brain-Derived Neurotrophic Factor (BDNF) and Neuregulin-1 (NRG-1) are crucial in sweat regulation.

Purpose of the Study:

• To investigate the therapeutic effects of Polydatin, a natural compound, on hyperhidrosis.
• To explore the role of Aquaporin 5 (AQP5) in Polydatin's mechanism of action.
• To assess the impact of Polydatin on sweat gland function and related molecular pathways.

Main Methods:

• A preclinical mouse model of hyperhidrosis was utilized.
• Mice were treated with varying doses and durations of Polydatin.
• Experiments included the use of Aqp5 knockout mice, analysis of gene and protein expression (AQP5, BDNF, NRG-1, NKCC1), and assessment of sweat gland cell responses to acetylcholine.

Main Results:

• Polydatin (50 mg/kg/day) significantly reduced sweat secretion in hyperhidrotic mice, independent of treatment duration.
• The therapeutic effect was dependent on AQP5, as it was absent in Aqp5 knockout mice.
• Polydatin downregulated AQP5, NKCC1, BDNF, and NRG-1 expression and inhibited acetylcholine-induced sweat gland cell proliferation.

Conclusions:

• Polydatin demonstrates efficacy in alleviating hyperhidrosis by targeting AQP5.
• The compound suppresses key neurologic factors involved in sweat regulation.
• Polydatin presents potential as a novel therapeutic agent for primary focal hyperhidrosis (PFH).