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

Molecules

Guang-Zhao Yang¹  Zhao-Jun Wang²  Feng Bai¹  Xiao-Jiang Qin²  Jing Cao¹  Ji-Yuan Lv¹  Ming-Sheng Zhang² 

[1] The Fist Clinical Hospital, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China; E-Mails:;Department of Pharmacology, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China; E-Mails:

关键词: epigallocatechin-3-gallate;    PM_2.5;    transcription factor nuclear factor E2-related factor 2;    heme oxygenase-1;    human umbilical vein endothelial cells;   

DOI  :  10.3390/molecules20046626

来源: mdpi

【 摘 要 】

Endothelial dysfunction and oxidative stress likely play roles in PM_2.5-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 (PM_2.5) is responsible for certain CVDs. The aim of the present study was to investigate whether EGCG could also inhibit PM_2.5-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). PM_2.5 (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 PM_2.5. 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 PM_2.5-induced oxidative stress injury by upregulating Nrf2/HO-1 via activation of the p38 MAPK and the ERK1/2 signaling pathways.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.