Quercetin (Que) Improved the Biological Activity of Preeclampsia Cells by Inhibiting Autophagy

Quercetin, a phytochemical sourced from botanicals, exhibits therapeutic potential for conditions including preeclampsia (PE); nevertheless, its precise mechanisms of action against this condition remain incompletely characterized. This investigation sought to explore the hypothesis that quercetin enhances cellular function in PE by suppressing autophagy during in vitro experiments. Within an oxygen-deprived setting, placental trophoblast cells were generated and subsequently exposed to varying doses of Quercetin (Que) alongside LY294002, a compound inhibiting PI3K activity. Cellular multiplication, programmed cell death, and invasive capacity were quantified. This evaluation employed tetrazolium salt (MTT) testing, fluorescence-activated cell sorting, Transwell chamber analysis, and scratch wound closure measurements. Furthermore, subcellular architecture was visualized through electron microscopic imaging, while immunoblot analysis determined expression levels of associated proteins. Relative to controls, HTR-8/SVneo cells exhibited markedly suppressed proliferation, invasive capacity, and 24-h/48-h scratch assay closure rates, alongside substantially elevated apoptotic activity (p < 0.001 throughout). Concomitantly, protein expression of PI3K, AKT, and mTOR was profoundly diminished, while autophagic activity was significantly amplified (p < 0.001 throughout). Subsequent Que intervention significantly enhanced cellular proliferation, invasion, and migratory potential in HTR-8/SVneo cultures, coupled with attenuated autophagy levels attributable to PI3K/AKT pathway activation. However, co-administration of Que with LY294002 substantially abrogated these Que-mediated effects. In conclusion, laboratory investigation demonstrates that Quercetin elevated the functional capabilities of placental trophoblast cells by modulating the phosphatidylinositol 3-kinase/protein kinase B signaling axis, concurrently suppressing autophagic processes.