Potential benefits of adlay on hyperandrogenism in human chorionic gonadotropin-treated theca cells and a rodent model of polycystic ovary syndrome

Journal of Functional Foods

Ya-Ting Wu¹  Kai-Lee Wang²  Tzong-Ming Shieh³  Mei-Jou Chen⁴  Shih-Min Hsia⁵  Chi-Hao Wu⁶  Wenchang Chiang⁶ 

[1] Sciences, Taipei Medical University, Taipei, Taiwan;;Center for Reproductive Medicine &Department of Dental Hygiene, College of Health Care, China Medical University, Taichung, Taiwan;Department of Obstetrics and Gynecology, National Taiwan University Hospital, Taipei, Taiwan;Institute of Food Science and Technology, College of Bioresources and Agriculture, National Taiwan University, Taipei, Taiwan;School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan;

关键词: Adlay;    Hyperandrogenemia;    Insulin resistance;    Polycystic ovary syndrome;    Dehydroepiandrosterone;   

DOI  :  

来源: DOAJ

【 摘 要 】

This study investigated the therapeutic potential of adlay on polycystic ovary syndrome (PCOS) and its possible underlying mechanism. The active anti-androgenic components in adlay were further analyzed. Rat ovarian theca cells were treated with human chorionic gonadotropin to stimulate androstenedione (AD) secretion. The ethyl acetate subfraction obtained from the ethanolic extract of adlay hull (AHE-EA) exerted superior efficacy against AD production. Four major constituents in AHE-EA, including 5,7-dihydroxychromone, liquiritigenin, isoliquiritigenin, and homoeriodictyol, were identified by HPLC–MS and exhibited strong inhibition against high AD levels. In a DHEA-induced PCOS rat model, administration of AHE-EA significantly decreased serum AD levels, improved hyperglycemia and insulin resistance, and attenuated oxidative stress and inflammatory responses in the ovaries. Histopathological morphology of ovarian tissues confirmed that AHE-EA could restore the estrus cycles and normal ovarian histology. Mechanistic characterization demonstrated that AHE-EA inhibited DHEA-induced hyperandrogenemia through modulate steroidogenic acute regulatory protein-related steroidogenesis in theca cells.

【 授权许可】

Unknown