Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells
Microcystin-LR (MC-LR), a cyanotoxin produced by cyanobacteria, induces oxidative stress in various types of cells. Prodigiosin, a red linear tripyrrole pigment, has been recently reported to have antimicrobial, antioxidative, and anticancer properties. How prodigiosin reacts to reactive oxygen spec...
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MDPI AG
2019-07-01
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Series: | Toxins |
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author | Jihua Chen Yuji Li Fuqiang Liu De-Xing Hou Jingjing Xu Xinying Zhao Fei Yang Xiangling Feng |
author_facet | Jihua Chen Yuji Li Fuqiang Liu De-Xing Hou Jingjing Xu Xinying Zhao Fei Yang Xiangling Feng |
author_sort | Jihua Chen |
collection | DOAJ |
description | Microcystin-LR (MC-LR), a cyanotoxin produced by cyanobacteria, induces oxidative stress in various types of cells. Prodigiosin, a red linear tripyrrole pigment, has been recently reported to have antimicrobial, antioxidative, and anticancer properties. How prodigiosin reacts to reactive oxygen species (ROS) induced by MC-LR is still undetermined. This study aimed to examine the effect of prodigiosin against oxidative stress induced by MC-LR in HepG2 cells. Ros was generated after cells were treated with MC-LR and was significantly inhibited with treatment of prodigiosin. In prodigiosin-treated cells, the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and Nrf2-related phase II enzyme heme oxygenase-1 (HO-1) were increased. Besides, prodigiosin contributed to enhance nuclear Nrf2 level and repressed ubiquitination. Furthermore, prodigiosin promoted Nrf2 protein level and inhibited ROS in Nrf2 knocked down HepG2 cells. Results indicated that prodigiosin reduced ROS induced by MC-LR by enhancing Nrf2 translocation into the nucleus in HepG2 cells. The finding presents new clues for the potential clinical applications of prodigiosin for inhibiting MC-LR-induced oxidative injury in the future. |
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language | English |
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spelling | doaj.art-0b491af2d98a40a7930dfd7bca74a1fa2022-12-22T04:03:58ZengMDPI AGToxins2072-66512019-07-0111740310.3390/toxins11070403toxins11070403Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 CellsJihua Chen0Yuji Li1Fuqiang Liu2De-Xing Hou3Jingjing Xu4Xinying Zhao5Fei Yang6Xiangling Feng7Xiangya School of Public Health, Central South University, Changsha 410128, Hunan, ChinaXiangya School of Public Health, Central South University, Changsha 410128, Hunan, ChinaDepartment of Public Health Emergency Treatment, Hunan Center for Disease Control and Prevention (CDC), Changsha 410005, Hunan, ChinaDepartment of Food Science and Biotechnology, Faculty of Agriculture, Kagoshima University, Kagoshima 890-0065, JapanXiangya School of Public Health, Central South University, Changsha 410128, Hunan, ChinaXiangya School of Public Health, Central South University, Changsha 410128, Hunan, ChinaXiangya School of Public Health, Central South University, Changsha 410128, Hunan, ChinaXiangya School of Public Health, Central South University, Changsha 410128, Hunan, ChinaMicrocystin-LR (MC-LR), a cyanotoxin produced by cyanobacteria, induces oxidative stress in various types of cells. Prodigiosin, a red linear tripyrrole pigment, has been recently reported to have antimicrobial, antioxidative, and anticancer properties. How prodigiosin reacts to reactive oxygen species (ROS) induced by MC-LR is still undetermined. This study aimed to examine the effect of prodigiosin against oxidative stress induced by MC-LR in HepG2 cells. Ros was generated after cells were treated with MC-LR and was significantly inhibited with treatment of prodigiosin. In prodigiosin-treated cells, the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and Nrf2-related phase II enzyme heme oxygenase-1 (HO-1) were increased. Besides, prodigiosin contributed to enhance nuclear Nrf2 level and repressed ubiquitination. Furthermore, prodigiosin promoted Nrf2 protein level and inhibited ROS in Nrf2 knocked down HepG2 cells. Results indicated that prodigiosin reduced ROS induced by MC-LR by enhancing Nrf2 translocation into the nucleus in HepG2 cells. The finding presents new clues for the potential clinical applications of prodigiosin for inhibiting MC-LR-induced oxidative injury in the future.https://www.mdpi.com/2072-6651/11/7/403prodigiosinmicrocystin-LRROSNrf2ubiquitination |
spellingShingle | Jihua Chen Yuji Li Fuqiang Liu De-Xing Hou Jingjing Xu Xinying Zhao Fei Yang Xiangling Feng Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells Toxins prodigiosin microcystin-LR ROS Nrf2 ubiquitination |
title | Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells |
title_full | Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells |
title_fullStr | Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells |
title_full_unstemmed | Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells |
title_short | Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells |
title_sort | prodigiosin promotes nrf2 activation to inhibit oxidative stress induced by microcystin lr in hepg2 cells |
topic | prodigiosin microcystin-LR ROS Nrf2 ubiquitination |
url | https://www.mdpi.com/2072-6651/11/7/403 |
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