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

Hee Yul Ahn; Chan Hyung Kim; Tae-Sun Ha

doi:10.4196/kjpp.2010.14.5.325

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Ahn, Kim, and Ha: Epigallocatechin-3-gallate Regulates NADPH Oxidase Expression in Human Umbilical Vein Endothelial Cells

Original Article

Korean J Physiol Pharmacol 2010;14(5):325-329.

Published online: 18 February 2010

DOI: https://doi.org/10.4196/kjpp.2010.14.5.325

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

Hee Yul Ahn^1,, Chan Hyung Kim¹, Tae-Sun Ha²

¹Department of Pharmacology, Chungbuk University, Cheongju 361-763, Korea

²Department of Pediatrics, College of Medicine, Chungbuk University, Cheongju 361-763, Korea

Corresponding to: Hee Yul Ahn, Department of Pharmacology, College of Medicine, Chungbuk University, 410, Seongbong-ro, Heungdeok-gu, Cheongju 361-763, Korea. (Tel) 82-43-261-2850, (Fax) 82-43-261-3178, (E-mail) hyahn@chungbuk.ac.kr

Received 15 September 2010 Revised 16 October 2010 Accepted 18 October 2010

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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^phox, p67^phox and p22^phox, induced by angiotensin II (Ang II) in human umbilical vein endothelial cells. Ang II increased the expression levels of p47^phox, p67^phox, and p22^phox, but EGCG counteracted this effect on p47^phox. 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.

Keywords: EGCG, NADPH oxidase, Angiotensin II, ROS, HUVEC

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Fig. 1.

Effect of Ang II treatment (100 nM, 0∼24 h) on the expression levels of NADPH oxidase subunits p47^phox, p67^phox and p22^phox in HUVECs. Summary data are shown as the mean±SEM. ^∗p<0.05 by Turkey's multiple comparison test.

Fig. 2.

Effect of EGCG on p47^phox expression in HUVECs treated with Ang II (100 nM) for 24 h, 30 min after treatment with EGCG (10∼50 μM).

Fig. 3.

Effect of EGCG (30–50 μM) on ROS induced by Ang II (100 nM) for 24 h in HUVECs. EGCG was pretreated 30 min before Ang II stimulation. Bars represent the mean±SEM. ^∗p<0.05 by Turkey's multiple comparison test.

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