| Description |
Elevated circulating fatty acids can cause oxidative stress and impair endothelial function, leading to cardiovascular disease. Quercetin, a flavonoid in fruits and vegetables, has been found to lower blood pressure in human and animal models, likely through protecting endothelial cell function. The aim of this study was to determine if quercetin protects endothelial cells challenged by a palmitate-induced oxidative state by activating Nrf2, an endogenous regulator of antioxidant defense. We hypothesized that increased Nrf2 activation by quercetin will prevent NFκB activation and result in lower inflammation in palmitate challenged cells. Confluent bovine aortic endothelial cells (BAECs) were treated with 1 μM quercetin and 500 μM palmitic acid either separately or concurrently for five hours. Nrf2 translocation, reactive oxygen species production (ROS), NFκB translocation, and mRNA expression of inflammatory markers were determined. Treatment with quercetin or palmitate alone increased nuclear translocation of Nrf2. However, concurrent treatment with quercetin and palmitate reduced Nrf2 back to control levels. There were no differences in ROS production between any treatment groups. NFκB nuclear translocation was increased with palmitate treatment alone and after co-treatment with palmitate and quercetin. mRNA expression of IL-8 and MCP-1 (markers of inflammation) increased after palmitate and after concurrent treatment with palmitate and quercetin. In conclusion, quercetin reduced nuclear Nrf2 during palmitate treatment, but exacerbated NFκB activation. Our data indicate that co-treatment of quercetin and palmitate prevents the activation of Nrf2, thereby increasing NFκB translocation and expression of inflammatory genes. These results do not support our initial hypothesis. |
