Paeoniflorin inhibits proliferation and promotes autophagy and apoptosis of sweat gland cells
- Yuan Xu
- Hong He
- Ping Li
- Hongwei Liu
Affiliations: Department of Plastic Surgery, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China, Health Care and Physical Examination Center, The First Affliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China, Department of Plastic Surgery, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, Guangdong 510080, P.R. China
- Published online on: November 16, 2021 https://doi.org/10.3892/etm.2021.10975
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Axillary bromhidrosis is sweat excreted by apocrine glands in the armpits, mouth corners and other parts. The clinical manifestation includes excessive sweating and heavy odor, leading to the growth of bacteria and skin disease. The present study investigated the mechanism underlying the effect of paeoniflorin (PF) in the treatment of bromhidrosis. PF was injected into the feet of rats, and the foot skin was dissected for histological analysis. Primary human sweat gland cells (hSGCs) were isolated from patients with bromhidrosis. After 24 h treatment with PF or 3‑methyladenine, the production of reactive oxygen species (ROS), autophagy, apoptosis, proliferation and cell cycle distribution were determined. PF induced nuclear pyknosis in rat SGCs. In vitro PF treatment inhibited cell proliferation with a 25% inhibitory concentration of 9.530 µM. Treatment with 9.530 µM PF for 24 h significantly increased apoptosis, ROS production and autophagy in hSGCs. PF promoted LC3B and Beclin 1 expression, but inhibited p62, phosphorylated (p)‑PI3K and p‑Akt expression. 3‑methyladenine treatment reversed PF‑induced changes in hSGCs. PF‑induced inhibition of hSGC proliferation was associated with ROS production, apoptosis, and autophagy. These findings provide a basis for treating bromhidrosis.