Benzo(α)pyrene induces oxidative stress and inflammation in human vascular endothelial cells through AhR and NF-κB pathways.

Exposure to polycyclic aromatic hydrocarbons (PAHs) contributes to development and exacerbation of atherosclerosis and cardiovascular disease. However, the underlying molecular mechanisms remain elusive. In the current study, the effect of benzo(α)pyrene (BaP) in human umbilical vein endothelial cells (HUVECs) was investigated, including its impact on apoptosis, cell viability, oxidative stress and inflammatory cytokine release. The role of aryl hydrocarbon receptor (AhR) and NF-κB signaling pathways involved in BaP-induced oxidative stress and inflammation was further investigated. Exposure to BaP induced cell apoptosis and terminal oxidative stress and inflammation responses in HUVECs. BaP also increased the expression of ICAM-1 and VCAM-1. Furthermore, BaP treatment of HUVECs activated AhR and NF-κB signaling pathways, and promoted reactive oxygen species generation and inflammatory cytokine release. The current findings suggest that BaP induced inflammatory cytokine release from HUVECs through oxidative stress accompanied with AhR and NF-κB pathway activation.