Journal of International Obstetrics and Gynecology ›› 2026, Vol. 53 ›› Issue (4): 468-473.doi: 10.12280/gjfckx.20251306

• Obstetric Physiology & Obstetric Disease:Original Article • Previous Articles     Next Articles

Reactive Oxygen Species Induce Mitochondrial Dysfunction and Inhibit Epithelial-Mesenchymal Transition in Trophoblasts in Preeclampsia

PENG Jing, LI Tian-jing, ZHANG Shu-yi, CHEN Miao-miao()   

  1. Department of Obstetrics, Maternal and Child Health Hospital of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430070, China (PENG Jing, CHEN Miao-miao);School of Medicine, Wuhan University of Science and Technology,, Wuhan 430070, China (LI Tian-jing, ZHANG Shu-yi)
  • Received:2025-11-25 Published:2026-08-15 Online:2026-08-25
  • Contact: CHEN Miao-miao E-mail:229312094@qq.com

Abstract:

Objective: To investigate the potential pathological mechanism of oxidative stress induced preeclampsia (PE) in HTR8/SVneo cell line. Methods: Placental tissue from one patient with severe PE was collected, and mitochondrial morphology was observed using biological transmission electron microscopy. HTR8/SVneo cells were treated with 10, 20, and 50 μmol/L H2O2 for 24 hours, with a control group established concurrently. Intracellular reactive oxygen species (ROS) levels, mitochondrial membrane potential, and the opening degree of the mitochondrial permeability transition pore (MPTP) were detected by flow cytometry in each group. Protein levels of epithelial-mesenchymal transition (EMT)-related marker proteins were measured by western blotting. Results: In the placental tissue from the severe PE patient, mitochondrial cristae appeared swollen, fractured, reduced, or disappeared (appearing vacuolated). In HTR8/SVneo cells, with increasing concentrations of H2O2, intracellular ROS levels gradually increased, the mitochondrial membrane potential gradually decreased, and MPTP opening degree progressively increased. The expression of the epithelial marker E-cadherin gradually increased, while the expression of the mesenchymal markers N-cadherin and Vimentin gradually decreased. Conclusions: This study preliminarily confirms altered mitochondrial morphology in the placental tissues of PE patients. Increased ROS levels may be involved in the pathogenesis of PE by inducing mitochondrial dysfunction and inhibiting the EMT process.

Key words: Pre-eclampsia, Reactive oxygen species, Membrane potential, Mitochondrial, Mitochondrial permeability transition pore, Epithelial-mesenchymal transition