Elucidation of pathophysiology for abnormal decidualization and development of its treatment

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To test this hypothesis, primary HESCs cultures were decidualized with 8-bromo-cAMP and medroxyprogesterone acetate in the presence or absence of rhCG at various concentrations. Hydrogen peroxide was used as a source of reactive oxygen species (ROS). rhCG conferred additional protection to oxidative cell death in decidualizing HESCs in a dose-dependent manner. In parallel, rhCG augmented the expression of the decidual transcription factor FOXO1 and its downstream target, the ROS scavenger superoxide dismutase 2 (SOD2). These results suggest that hCG improves the uterine environment upon implantation by suppressing apoptotic responses the maternal decidua under oxidative stress conditions.