Epigallocatechin-3-gallate Regulates NADPH Oxidase Expression in Human Umbilical Vein Endothelial Cells

Abstract

Vascular NADPH oxidase plays a pivotal role in producing superoxide in endothelial cells and thus acts in the initiation and development of inflammatory cardiovascular diseases such as atherosclerosis. Epigallocatechin-3-gallate (EGCG), the major catechin derived from green tea, has multiple beneficial effects for treating cardiovascular disease but the effect of EGCG on the expression of vascular NADPH oxidase remains unknown. In this study, we investigated the mechanism(s) by which EGCG might inhibit the expression of subunits of NADPH oxidase, namely p47 . Moreover, EGCG did not affect the production of reactive oxygen species induced by Ang II. These data suggest a novel mechanism whereby EGCG might provide direct vascular benefits for treating inflammatory cardiovascular diseases.

Epigallocatechin‐3‐Gallate Inhibits Collagen Production of Nasal Polyp‐Derived Fibroblasts

“…An antioxidative function has been proposed as one of the mechanisms for the anti‐tumor and anti‐atherogenic effects of catechins (da Silva et al ., ; Zhang et al ., ). In a study of vascular NADPH oxidase, EGCG reduced the expression of NADPH oxidase and ROS production in human umbilical vein endothelial cells (Ahn et al ., ). NADPH oxidase is also considered a major source of ROS in TGF‐β1 induced NPDFs.…”

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

“…Moreover, the role of Ang II in mediating HUVEC responses to oxidative stress has been investigated [31,32]. Although past studies have confirmed that EGCG inhibits Ang II-induced adhesion molecule levels in HUVECs [33,34], understanding of the underlying molecular mechanisms remains limited. Our study suggested that EGCG is able to attenuate Ang II-enhanced HUVEC injury, at least in part, via the activation of Nrf2 signaling.…”

The dietary flavonol quercetin ameliorates angiotensin II‐induced redox signaling imbalance in a human umbilical vein endothelial cell model of endothelial dysfunction via ablation of p47phox expression

“…For this study primary vascular endothelial cells (human umbilical vein endothelial cells; HUVEC) have been used rather than endothelial cell lines, which have been reported to vary in characteristics quite dramatically when compared to ex vivo tissues. HUVEC are well characterized, relatively easily accessible, primary cells that have been reported to exhibit key endothelial cell functions, and are extensively used in the study of the effects of dietary chemicals upon cardiovascular biology and diseases . Specifically, we have assessed the effects of quercetin on NO˙ availability, O 2 ·− production and NADPH oxidase subunit protein levels and activity.…”