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J Vasc Res. 2017;54(5):299-308. doi: 10.1159/000479873. Epub 2017 Sep 23.

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.

Author information

1
Department of Cardiology, The First People's Hospital of Yunnan, Kunming, China.

Abstract

INTRODUCTION:

This study aimed to investigate whether epigallocatechin-3-gallate (EGCG) shows antioxidant activity against angiotensin II (Ang II)-induced human umbilical vein endothelial cell (HUVEC) apoptosis.

MATERIALS AND METHODS:

The viability of HUVECs was revealed by MTT and LDH assay. The cell apoptosis was detected by FITC-PI assay. A fluorescent probe assay was used to measure the reactive oxygen species (ROS) generation in HUVECs. Mitochondrial permeability transition pore (MPTP) opening, mitochondrial membrane potential, and caspase-3, -4, -8, -9 activities were also measured.

RESULTS:

We found that Ang II treatment increased the generation of ROS, enhanced MPTP opening and cytochrome c release, activated caspase-3/9, and consequently induced HUVEC apoptosis. EGCG treatment-suppressed Ang II induces the oxidative stress of HUVECs and mitochondria-related cell apoptosis. We also showed that the antioxidant activity pathway, including cytochrome c release, MPTP opening, and caspase-3/9 activation, is a key endogenous defensive system in HUVECs, provoking Ang II exposure. Our study revealed that increased expression of Nrf2 by EGCG could partially repress Ang II-induced injury effects.

CONCLUSIONS:

All of our findings indicated that EGCG treatment provides a protective effect for Ang II-induced HUVEC apoptosis by decreasing oxidative stress and ameliorating mitochondrial injury.

KEYWORDS:

Angiotensin II; Epigallocatechin-3-gallate; Human umbilical vein endothelial cells; Nrf2; Oxidative stress

PMID:
28942440
DOI:
10.1159/000479873
[Indexed for MEDLINE]

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