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Updated: Sep 13, 2026
A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
Published on: October 2, 2018
Cinnamaldehyde Attenuates Dehydroepiandrosterone-induced Apoptosis and Inflammatory Responses in a KGN Cell Model of
Jinyan Gao1,2, Xiaodan Weng3,4, Jiali Cheng3,4
1Department of Gynecology and Obstetrics, Qiantang Campus, Zhejiang Provincial Hospital of Integrated Chinese and Western Medicine, No. 98 Yilong Road, Qiantang District, Hangzhou, 311225, Zhejiang Province, China. jinyan_g225@163.com.
Abstract:
Polycystic ovary syndrome (PCOS) is a complex reproductive and metabolic disorder characterized in part by chronic low-grade inflammation and granulosa-cell dysfunction. New interventions that protect granulosa cells from hyperandrogenic injury are needed. Cinnamaldehyde (CA), a major bioactive component of cinnamon, has anti-inflammatory and cytoprotective properties; however, its effects in PCOS-related cell models remain unclear. We evaluated CA in human KGN granulosa-like cells treated with dehydroepiandrosterone (DHEA) to establish an in vitro PCOS-like model. CA increased cell viability and EdU incorporation in DHEA-treated cells, reduced the production and expression of TNF-α, IL-1β, and IL-6, and decreased apoptosis. CA also increased PI3K and Akt phosphorylation relative to DHEA treatment alone. These findings indicate that CA attenuates DHEA-induced inflammatory and apoptotic injury in KGN cells and that its effects are associated with restoration of PI3K/Akt signaling. CA therefore warrants further mechanistic evaluation as a potential modulator of PCOS-related granulosa-cell dysfunction.
