Fetal growth restriction (FGR) is characterized by the inability of the fetus to achieve its growth potential due to pathological factors, most commonly impaired placental trophoblast cell function. Currently, effective prevention and treatment methods of FGR are limited. We aimed to explore the pathogenesis of FGR and provide potential strategies for mitigating its occurrence. The case-control study compared AQP3 expression in placental trophoblast cells of pregnant women with FGR and those with normal pregnancies. Then mouse FGR models were induced via cadmium exposure, and placental trophoblast cells (JEG-3) were similarly treated. The study assessed the effects of Sodium tanshinone IIA sulfonate (STS) and the role of the PI3K/Akt pathway in improving AQP3 expression and trophoblast cell function. Placental trophoblast cells in FGR cases exhibited significantly reduced AQP3 expression. AQP3-knockdown cells displayed dysfunction. Cadmium exposure in mice and JEG-3 cells led to decreased AQP3 expression and trophoblast cell dysfunction, both of which were ameliorated by STS. Fetal mouse weight increased with STS treatment. STS upregulated AQP3 expression and improved trophoblast cell function in AQP3-knockdown cells. Inhibiting the PI3K/Akt pathway diminished STS's beneficial effects. ThereforeSTS may enhance AQP3 expression in placental trophoblast cells affected by FGR through the activation of the PI3K/Akt pathway, ultimately bolstering placental trophoblast cell function and alleviating FGR. As above, STS appears to be a potential therapeutic agent for alleviating FGR.
Keywords: AQP3; fetal growth restriction; placental trophoblast cells; sodium tanshinone IIA sulfonate.
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