Cinnamaldehyde Attenuates Dehydroepiandrosterone-induced Apoptosis and Inflammatory Responses in a KGN Cell Model of Polycystic Ovary Syndrome.

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.