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Article

Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells

1
Xiangya School of Public Health, Central South University, Changsha 410128, Hunan, China
2
Department of Public Health Emergency Treatment, Hunan Center for Disease Control and Prevention (CDC), Changsha 410005, Hunan, China
3
Department of Food Science and Biotechnology, Faculty of Agriculture, Kagoshima University, Kagoshima 890-0065, Japan
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Received: 24 June 2019 / Revised: 8 July 2019 / Accepted: 9 July 2019 / Published: 12 July 2019
(This article belongs to the Collection Toxicological Challenges of Aquatic Toxins)
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. View Full-Text
Keywords: prodigiosin; microcystin-LR; ROS; Nrf2; ubiquitination prodigiosin; microcystin-LR; ROS; Nrf2; ubiquitination
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MDPI and ACS Style

Chen, J.; Li, Y.; Liu, F.; Hou, D.-X.; Xu, J.; Zhao, X.; Yang, F.; Feng, X. Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells. Toxins 2019, 11, 403. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins11070403

AMA Style

Chen J, Li Y, Liu F, Hou D-X, Xu J, Zhao X, Yang F, Feng X. Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells. Toxins. 2019; 11(7):403. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins11070403

Chicago/Turabian Style

Chen, Jihua, Yuji Li, Fuqiang Liu, De-Xing Hou, Jingjing Xu, Xinying Zhao, Fei Yang, and Xiangling Feng. 2019. "Prodigiosin Promotes Nrf2 Activation to Inhibit Oxidative Stress Induced by Microcystin-LR in HepG2 Cells" Toxins 11, no. 7: 403. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins11070403

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