Epigallocatechin-3-gallate attenuates microcystin-LR induced oxidative stress and inflammation in human umbilical vein endothelial cells

被引：29
作者：
Shi, Jun [1 ]
Deng, Huiping [1 ]
Pan, Huichao [2 ]
Xu, Yinjie [2 ]
Zhang, Min [2 ]
机构：
[1] Tongji Univ, Coll Environm Sci & Engn, Key Lab Yangtze River Water Environm, Shanghai, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, TongRen Hosp, Div Cardiol, 1111 Xianxia Rd, Shanghai 200336, Peoples R China
来源：
CHEMOSPHERE | 2017年 / 168卷
关键词：
Microcystin-LR; Epigallocatechin-3-gallate; Human umbilical vein endothelial cells; Reactive oxygen species; Angiogenesis; NF-KAPPA-B; ZEBRAFISH DANIO-RERIO; IN-VIVO; TNF-ALPHA; EXPOSURE; (-)-EPIGALLOCATECHIN-3-GALLATE; GROWTH; LUNG; INHIBITION; ACTIVATION;
D O I：
10.1016/j.chemosphere.2016.10.037
中图分类号：
X [环境科学、安全科学];
学科分类号：
08 ; 0830 ;
摘要：
Epigallocatechin-3-gallate (EGCG) has been shown to possess anti-inflammatory effects. Microcystin-LR (MC-LR) is a potent toxin and our past research suggested that it also mediated human umbilical vein endothelial cell (HUVEC) injury. The aim of this study was to investigate the effects of EGCG on MC-LR-induced oxidative stress and inflammatory responses in HUVECs. HUVECs were stimulated with MC-LR in the presence or absence of EGCG. MC-LR (40 AM) significantly increased cell death and decreased cell viability, migration, and tube formation, whereas EGCG (50 mu M) inhibited these effects. Furthermore, the results indicated that EGCG inhibited the production of reactive oxygen species (ROS), tumor necrosis factor alpha (TNF-alpha), and interleukin-6 (IL-6) in MC-LR-stimulated HUVECs. Compared with MC-LR, EGCG significantly increased superoxide dismutase (SOD) and glutathione (GSH) levels and decreased malondialdehyde (MDA) levels. Moreover, the analysis indicated that EGCG suppressed MC-LR-induced NF-kappa B activation. In conclusion, the effects of EGCG were associated with inhibition of the NF-kappa B signaling pathway, which resulted in decreased ROS and TNF-alpha, thereby attenuating MC-LR-mediated oxidative and inflammatory responses. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码：25 / 31
页数：7
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