Brazilian green propolis attenuates endothelial dysfunction and oxidative stress in a preeclampsia model in vitro

Brazilian green propolis is notable for its ability to modulate immune cells. In preeclampsia (PE), endothelial dysfunction is caused by the release of damage-associated molecular patterns, oxidative stress, elevated pro-inflammatory cytokines, and adhesion molecules. This study aimed to evaluate the effects of propolis on biomarkers of endothelial dysfunction and oxidative stress using human umbilical vein endothelial cells (HUVECs).

HUVECs were cultured with plasma from early-onset (EOPE; n = 16) or late-onset (LOPE; n = 16) preeclamptic women, as well as from normotensive pregnant women (NT; n = 20). Cells were stimulated with HMGB1 and Hsp70, with or without propolis. This human endothelial cell-based model was used to investigate the disease-associated mechanisms relevant to PE and to evaluate propolis effects. The expression of Flt-1, VEGFR2, endoglin, E-selectin, ICAM-1 and VCAM-1 was assessed by flow cytometry. HMGB1, Hsp70, IL-6, IL-8, sFlt-1, sEng, and VEGF were measured by ELISA, and reactive oxygen species (ROS) by fluorescence assay.

Propolis reduced endothelial activation markers, ROS generation, IL-6 and IL-8 in both PE plasma-activated cells and DAMP-stimulated cell cultures. Propolis restored angiogenic balance by increasing VEGF levels while reducing sFlt-1 and sEng levels.

Propolis attenuated endothelial dysfunction, inflammatory activation, oxidative stress, and angiogenic imbalance.