Bisphenol A‐Induced Vascular Endothelial Dysfunction: Protective Effects of <i>Nigella sativa</i> Oil and Thymoquinone

In the present study, the effectiveness of <i>Nigella sativa</i> oil (NSO) and thymoquinone (TQ), a major ingredient in <i>Nigella sativa</i>, on vascular endothelial dysfunction induced by bisphenol A (BPA) was assessed. Male Wistar rats were exposed to NSO (84 μL/kg), TQ (2 mg/kg), BPA (10 mg/kg), BPA plus NSO (21, 42, or 84 μL/kg), or BPA plus TQ (0.5, 1, or 2 mg/kg) (<i>n</i> = 6 per group). After the treatment period, oxidative and nitrosative stress markers in both aorta and human umbilical vein endothelial cells (HUVECs) were evaluated. In HUVECs, protein levels of phospho-endothelial nitric oxide synthase (p-eNOS) and adhesion molecules (vascular cell adhesion molecule-1 [VCAM-1] and E-selectin) were measured. In addition, contractile responses to potassium chloride (KCl) and phenylephrine (PE) and relaxant responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were evaluated in the rat aorta. BPA caused a significant increase in aorta lipid peroxidation, elevated reactive oxygen species (ROS), nitric oxide (NO), VCAM-1, and p-eNOS in HUVECs, and decreased aorta responses to KCl and PE. These changes were ameliorated by NSO and TQ administration. Furthermore, NSO and TQ alone increased the vasorelaxation responses induced by ACh and SNP. These findings suggest that NSO and TQ can protect the vascular endothelium against BPA-induced damage, probably resulting from their antioxidant activity, as well as their ability to attenuate cell adhesion molecules.