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Molecules 2015, 20(4), 6626-6639; doi:10.3390/molecules20046626

Epigallocatechin-3-Gallate Protects HUVECs from PM2.5-Induced Oxidative Stress Injury by Activating Critical Antioxidant Pathways

1
The Fist Clinical Hospital, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China
2
Department of Pharmacology, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China
3
Department of Physiology, Shanxi Province Key Laboratory of Cellular Physiology, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China
*
Authors to whom correspondence should be addressed.
Academic Editor: Derek J. McPhee
Received: 27 February 2015 / Revised: 3 April 2015 / Accepted: 8 April 2015 / Published: 14 April 2015
(This article belongs to the Section Medicinal Chemistry)
View Full-Text   |   Download PDF [1561 KB, uploaded 14 April 2015]   |  

Abstract

Endothelial dysfunction and oxidative stress likely play roles in PM2.5-induced harmful effects. Epigallocatechin-3-gallate (EGCG), the major polyphenolic constituent of green tea, is a potent antioxidant that exerts protective effects on cardiovascular diseases (CVDs) in part by scavenging free radicals. The exposure to ambient fine particulate matter (PM2.5) is responsible for certain CVDs. The aim of the present study was to investigate whether EGCG could also inhibit PM2.5-induced oxidative stress by activating the nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway in human umbilical vein endothelial cells (HUVECs). PM2.5 (200 μg/mL) increased both cell death and intracellular ROS levels significantly, whereas EGCG (50–400 μM) inhibited these effects in a concentration-dependent manner. Western blotting and PCR demonstrated that EGCG increased Nrf2 and HO-1 expression in HUVECs that had been exposed to PM2.5. PD98059 (a selective inhibitor of extracellular signal regulated kinase [ERK]-1/2) and SB203580 (a selective inhibitor of p38 MAPK), but not SP600125 (a selective inhibitor of c-jun N-terminal kinase [JNK]), attenuated the EGCG-induced Nrf2 and HO-1 expression. In addition, silencing Nrf2 abolished EGCG-induced Nrf2 and HO-1 upregulation and enhancement of cell viability. The present study suggests that EGCG protects HUVECs from PM2.5-induced oxidative stress injury by upregulating Nrf2/HO-1 via activation of the p38 MAPK and the ERK1/2 signaling pathways. View Full-Text
Keywords: epigallocatechin-3-gallate; PM2.5; transcription factor nuclear factor E2-related factor 2; heme oxygenase-1; human umbilical vein endothelial cells epigallocatechin-3-gallate; PM2.5; transcription factor nuclear factor E2-related factor 2; heme oxygenase-1; human umbilical vein endothelial cells
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Yang, G.-Z.; Wang, Z.-J.; Bai, F.; Qin, X.-J.; Cao, J.; Lv, J.-Y.; Zhang, M.-S. Epigallocatechin-3-Gallate Protects HUVECs from PM2.5-Induced Oxidative Stress Injury by Activating Critical Antioxidant Pathways. Molecules 2015, 20, 6626-6639.

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