Bisphenol A (BPA) is widely used in industrial production.It is closely related to the growth and development of the nervous system, and can enter the fetal circulation through the placental barrier, and can be secreted through breast milk.The development of nervous system is very important in fetus and neonatal period.The purpose of this study is to investigate the effects of different doses of BPA on learning and memory function of nervous system in rats.Pregnant rats were randomly divided into three treatment groups (control group, 5 mg/kg/d, 50 mg/kg/d).All animals received BPA from the discovery of pregnancy to 21 days after birth.Results had shown that after high concentration BPA exposure, the increase of PS amplitude and f-EPSP slope in hippocampal CA1 area of male offspring was lower than that of control group.High concentration of BPA could inhibit Nestin, Cyclin D1, bcl-2 and Rac1 in male offspring rats and the expression of bax and RhoA was promoted by BPA.In summary, our study indicated that BPA exposure during pregnancy and lactation could impair the hippocampal function of male offspring by affecting the growth and apoptosis of hippocampal neurons, which might be due to the abnormal regulation of RhoA and Rac1.

Preeclampsia (PE) is a systemic complication that occurs after the 20th week of gestation and is characterized by the onset of hypertension and proteinuria. Dysregulated circulating microRNA (miRNA) has usually been noted in PE. Understanding the release profile and bioactivity of placental exosomes is a promising mode of identifying dysregulated miRNA, which may be useful biomarkers of PE. Herein, we aimed to investigate the role of placental exosomes and their miRNA cargo miR-15a-5p in PE. miR-15a-5p was found upregulated in exosomes isolated from maternal plasma of PE pregnant women as compared to those from normal pregnant women. Placental exosomes derived from PE pregnant women suppressed the proliferation and invasion of HTR-8/SVneo cells but promoted cell apoptosis, which was dictated by their cargo miR-15a-5p. Further investigation showed that exosomal miR-15a-5p inhibited the activation of the PI3K/AKT pathway by down-regulating CDK1, thus suppressing HTR-8/SVneo cell proliferation, invasion, and apoptosis. In vivo analysis demonstrated that placental exosomes treated with miR-15a-5p inhibitor attenuated histopathologic changes and apoptosis in the placenta of PE mice. In conclusion, these results provided evidence that transfer of miR-15a-5p by placental exosomes could be a promising therapeutic target to combat PE.