Investigating the Effect of Di(2-ethylhexyl) Phthalate (DEHP) Exposure on the Pathophysiology of Preeclampsia Using the Reduced Uterine Perfusion Pressure (RUPP) Rat Model

• Grant number: 25/14354-6
• Support Opportunities: Scholarships abroad - Research Internship - Post-doctor
• Start date: September 29, 2025
• End date: September 28, 2026
• Field of knowledge: Health Sciences - Medicine - Maternal and Child Health
• Principal Investigator: Valeria Cristina Sandrim
• Grantee: Bárbara Campos Jorge
• Supervisor: Ana Carolina Taveiros Palei
• Host Institution: Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil
• Institution abroad: University of Mississippi Medical Center (UMMC), United States
• Associated to the scholarship: 23/06651-5 - Study of endocrine disruptors (EDRs) and sex hormones in PE., BP.PD

Abstract

Preeclampsia (PE) is a complex hypertensive disorder of pregnancy characterized by abnormal placental development, endothelial dysfunction, and systemic inflammation. Emerging evidence suggests that exposure to environmental endocrine-disrupting chemicals (EDCs), such as phthalates, may contribute to the development and severity of PE. Di(2-ethylhexyl) phthalate (DEHP), a widely used plasticizer, has been implicated in disrupting angiogenic signaling and vascular integrity during pregnancy. This project aims to investigate the effects of DEHP exposure on the pathophysiology of PE using the Reduced Uterine Perfusion Pressure (RUPP) rat model - a well-established experimental model that mimics key clinical features and biomarkers of human PE. Pregnant rats will be divided into four experimental groups: normotensive controls, DEHP-exposed normotensive rats, RUPP rats, and RUPP rats with DEHP exposure. Maternal blood pressure, cardiac function, hormone levels, and key mediators of angiogenesis, inflammation, and oxidative stress along with histological analysis of the heart, aorta, and placenta, will be evaluated. We hypothesize that DEHP exposure will induce PE-like features in normotensive rats and exacerbate PE severity in the RUPP model through disrupted vascular signaling and hormonal imbalances. These findings will provide novel mechanistic insights into the environmental contributions to PE (AU)