Low molecular weight heparins promote migration and invasion of trophoblast cells through regulating the PI3K/AKT signaling pathway.

Pregnant women confront a high risk of mortality due to preeclampsia (PE), which also results in severe challenges for newborns. Due to their efficient properties and minimal side effects, low molecular weight heparins (LMWHs) are extensively utilized by optimizing their molecular size. Nevertheless, there have been no reports regarding the alleviating effect of LMWHs on PE and the molecular mechanism underlying it. To examine the therapeutic impact of LMWHs on PE, we initially created a PE rat model and assessed the advantages of LMWHs on PE through Western blot, immunofluorescence, TUNEL, 24-h proteinuria determination, and other techniques. Furthermore, we examined the in vitro molecular mechanism of LMWHs therapy on PE using CCK-8, Transwell, Flow cytometry, Wound healing assay, and other techniques. LMWHs, when used in vivo, reduced the rise in blood pressure and 24-h proteinuria in rat models of PE. Additionally, they prevented trophoblast cell apoptosis in these rat models. In vitro, LMWHs demonstrated a significant ability to enhance the migration and invasion of HTR-8 and JEG-3 cells. Mechanistically, LMWHs mitigate the development of PE by activating the PI3K/AKT signaling pathway. According to our findings, the activation of the PI3K/AKT signaling pathway by LMWHs appears to provide relief for PE. Therefore, we have compelling evidence supporting the use of LMWHs as an efficient treatment for PE.