Sulforaphane improves vascular reactivity in mouse and human arteries after “preeclamptic-like” injury

The widespread maternal endothelial dysfunction that underlies the manifestations of preeclampsia is thought to arise from excessive placental production of antiangiogenic factors and enhanced oxidative stress. Therefore, we assessed whether the natural antioxidant sulforaphane could improve vascular function. Cell viability of human umbilical vein endothelial cells (HUVECs) was assessed after 24 or 48 h in normoxia (20% O2) or hypoxia (1% O2) with or without sulforaphane. To model vascular dysfunction associated with preeclampsia, mouse mesenteric arteries were incubated in trophoblast conditioned media (TCM), and human omental arteries incubated in preeclamptic explant media (PEM) with or without sulforaphane. Both media are rich in antiangiogenic compounds associated with preeclampsia. TCM was generated from primary cytotrophoblast cells from term placentae of normotensive, while PEM was generated from explants from preeclamptic women. Reactivity was assessed by wire myography. sulforaphane's actions as a vasodilator were also investigated. Under conditions of hypoxia, sulforaphane improved HUVEC viability. In mouse mesenteric arteries, sulforaphane reduced contraction evoked by potassium (p