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首页> 外文期刊>Environmental Pollution >Epigallocatechin-3-gallate attenuates microcystin-LR-induced apoptosis in human umbilical vein endothelial cells through activation of the NRF2/HO-1 pathway
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Epigallocatechin-3-gallate attenuates microcystin-LR-induced apoptosis in human umbilical vein endothelial cells through activation of the NRF2/HO-1 pathway

机译：Epigallocatechin-3-gallate通过激活NRF2 / HO-1途径减轻微囊藻毒素LR诱导的人脐静脉内皮细胞凋亡

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摘要

Our previous study showed that the tea extract, epigallocatechin-3-gallate (EGCG), protects against microcystin-LR (MC-LR) -mediated apoptosis of human umbilical vein endothelial cells (HUVECs); however, the mechanism underlying MC-LR-induced HUVEC apoptosis remains incompletely understood. In this study, we investigated whether the nuclear factor erythroid-like 2 (NRF2)/heme oxygenase-1 (HO-1) pathway, which regulates antioxidant transcriptional regulation of oxidative stress and apoptosis, is involved in this process. Mitochondrial membrane potential (MMP) and caspase-3/-9 activities were evaluated in HUVECs by JC-1 staining and colorimetric activity assay, and a DCFH-DA fluorescent probe assay was used to quantitate reactive oxygen species (ROS) generation. The effects of MC-LR, EGCG, NF2, and HO-1 on HUVEC apoptosis were explored by western blotting and small interfering RNA (siRNA) analyses. MC-LR treatment downregulated HUVEC mitochondrial membrane potential, and decreased levels of cytochrome c release and activated caspase-3/-9, ROS generation, consequently inducing HUVEC apoptosis. EGCG treatment attenuated MC-LR-mediated HUVEC oxidative stress and mitochondria-related apoptosis. EGCG induced NRF2/HO-1 expression and activation in MC-LR treated HUVECs, while downregulation of NRF2/HO-1 by specific siRNAs revealed that NRF2/HO-1 signaling was involved in EGCG attenuation of MC-LR-induced HUVEC apoptosis. Our findings indicate that EGCG treatment protects against MC-LR-mediated HUVEC apoptosis via activation of NRF2/HO-1 signaling. (C) 2018 Elsevier Ltd. All rights reserved.
机译：我们以前的研究表明，茶提取物Epigallocatechin-3-gallate（EGCG）可防止微囊藻毒素LR（MC-LR）介导的人脐静脉内皮细胞（HUVEC）凋亡。然而，仍不清楚MC-LR诱导的HUVEC凋亡的潜在机制。在这项研究中，我们调查了核因子类红细胞样2（NRF2）/血红素加氧酶-1（HO-1）通路是否参与此过程，该通路调节氧化应激和细胞凋亡的抗氧化剂转录调控。通过JC-1染色和比色活性测定法评估HUVEC中的线粒体膜电位（MMP）和caspase-3 / -9活性，并使用DCFH-DA荧光探针测定法定量活性氧（ROS）的产生。通过蛋白质印迹和小干扰RNA（siRNA）分析，探讨了MC-LR，EGCG，NF2和HO-1对HUVEC细胞凋亡的影响。 MC-LR治疗下调HUVEC线粒体膜电位，降低细胞色素c释放水平并激活caspase-3 / -9，ROS生成，从而诱导HUVEC凋亡。 EGCG处理可减轻MC-LR介导的HUVEC氧化应激和线粒体相关的细胞凋亡。 EGCG诱导了MC-LR治疗的HUVEC中NRF2 / HO-1的表达和激活，而特异性siRNA下调NRF2 / HO-1则表明NRF2 / HO-1信号参与了MCCG诱导的HUVEC凋亡的EGCG减弱。我们的发现表明，EGCG治疗可通过激活NRF2 / HO-1信号传导来防御MC-LR介导的HUVEC细胞凋亡。 （C）2018 Elsevier Ltd.保留所有权利。

著录项

  • 来源
    《Environmental Pollution》 |2018年第8期|466-472|共7页
  • 作者

    Shi Jun; Zhang Min; Zhang Libin; Deng Huipin;

  • 作者单位

    Tongji Univ, Coll Environm Sci & Engn, State Key Lab Pollut Control & Resource Reuse, Shanghai, Peoples R China;

    Shanghai Jiao Tong Univ, TongRen Hosp, Div Cardiol, Sch Med, 1111 Xianxia Rd, Shanghai 200336, Peoples R China;

    First Peoples Hosp Yunnan Prov, Dept Thorac Surg, Kunming 650031, Yunnan, Peoples R China;

    Tongji Univ, Coll Environm Sci & Engn, State Key Lab Pollut Control & Resource Reuse, Shanghai, Peoples R China;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Epigallocatechin-3-gallate; Microcystin-LR; Human umbilical vein endothelial cells; Oxidative stress; NRF2;

    机译：表没食子儿茶素-3-没食子酸酯;微囊藻毒素-LR;人脐静脉内皮细胞;氧化应激;NRF2;

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