肥胖合并妊娠期糖尿病产妇胎盘滋养层细胞凋亡机制OACSTPCD

Objective To explore the mechanism by which hyperglycemia and hyperlipidemia promote apoptosis of placental trophoblasts in obese puerperae with gestational diabetes mellitus.Methods The placentas of 20 healthy(NC)puerperae,20 gestational diabetes mellitus(GDM)puerperae,20 obese(OB)puerperae and 20 obese puerperae combined with gestational diabetes mellitus(OB+GDM)were collected at the Second Hospital of Tianjin Medical University between January 2020 and January 2023.Placental pathology was detected via HE staining and the expressions of apoptosis-related proteins by immunohistochemistry.The expressions of mammalian sterile 20-like kinase 1(MST1),c-Jun N-terminal kinase(JNK),Bcl-2 associated X protein(BAX),B-cell lymphoma-2(Bcl-2),cysteinyl aspartate specific proteinase(caspase 3)and other apoptosis-related proteins were detected by Western blotting.Results HE staining revealed that hyperglycemia and hyperlipidemia could lead to a relative decrease and varying sizes of syncytial trophoblasts and cytotrophoblasts in placentas.The TUNEL method found that hyperglycemia and hyperlipidemia led to increased apoptosis in trophoblasts,particularly in syncytial trophoblasts,with the most pronounced apoptosis in the obese combined with GDM group.Immunohistochemical detection of placentas revealed that hyperglycemia and hyperlipidemia could increase the expressions of apoptosis-related proteins MST1 and JNK.The regulatory pathway of MST1-JNK-BAX-CASP3 apoptosis was found to be involved in the apoptotic process of placental trophoblasts by Western blotting.Conclusion The placental trophoblasts of obese women with gestational diabetes mellitus may overproduce reactive oxygen species in the internal environment formed by hyperglycemia and hyperlipidemia,which mediates the apoptosis of placental trophoblasts through the regulatory pathway of MST1-JNK-BAX-CASP3 apoptosis,thus affecting the placental function.