EGCG reduces Ang II‐induced NAD(P)H oxidase and NO synthase expression in HUVECs

Abstract

Atherosclerosis is a chronic systemic disease of the vasculature with an inflammatory component. The impairment of vascular endothelial cell function which is an important determinant of atherosclerosis progression is in part due to increased release of reactive oxygen species (ROS). Angiotensin II (Ang II) causes endothelial dysfunction by increasing NAD(P)H oxidase‐mediated vascular superoxide production. Epigallocatechin‐3‐gallate (EGCG), the major bioactive polyphenol present in green tea and a potent antioxidant, has been reported to lower the risk of cardiovascular diseases such as atherosclerosis and hypertension. In this study, we investigated the effects of EGCG on Ang II‐induced expression of NAD(P)H oxidase and nitric oxide synthase (NOS), which may contribute to oxidative stress. We observed that Ang II stimulated mRNA and protein expression of NAD(P)H oxidase subunit and iNOS in human umbilical vein endothelial cells (HUVECs). EGCG inhibited Ang II‐induced expression of NAD(P)H oxidase subunit and iNOS in a concentration‐dependent manner. However, EGCG did not affect Ang II‐induced ROS production. Surprisingly, EGCG itself produced ROS in HUVECs. These results suggest that anti‐atherosclerotic activity of EGCG is likely not due to decreased ROS formation although there may be some benefit through inhibition of expression of NAD(P)H oxidase and NOS induced by Ang II.