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Polydatin Protects Bovine Mammary Epithelial Cells against Zearalenone-Induced Apoptosis by Inhibiting Oxidative Responses and Endoplasmic Reticulum Stress

Zearalenone (ZEA) is a mycotoxin of the Fusarium genus that can cause endoplasmic reticulum (ER) stress and Apoptosis in bovine mammary epithelial cells (MAC-T). Polydatin (PD), a glycoside purified from Polygonum cuspidatum, has antioxidant properties. This study aimed to explore whether PD can all...

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Autores principales: Fu, Yurong, Jin, Yongcheng, Shan, Anshan, Zhang, Jing, Tang, Hongyu, Shen, Jinglin, Zhou, Changhai, Yu, Hao, Fang, Hengtong, Zhao, Yun, Wang, Junxiong, Tian, Yue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7915214/
https://www.ncbi.nlm.nih.gov/pubmed/33562867
http://dx.doi.org/10.3390/toxins13020121
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author Fu, Yurong
Jin, Yongcheng
Shan, Anshan
Zhang, Jing
Tang, Hongyu
Shen, Jinglin
Zhou, Changhai
Yu, Hao
Fang, Hengtong
Zhao, Yun
Wang, Junxiong
Tian, Yue
author_facet Fu, Yurong
Jin, Yongcheng
Shan, Anshan
Zhang, Jing
Tang, Hongyu
Shen, Jinglin
Zhou, Changhai
Yu, Hao
Fang, Hengtong
Zhao, Yun
Wang, Junxiong
Tian, Yue
author_sort Fu, Yurong
collection PubMed
description Zearalenone (ZEA) is a mycotoxin of the Fusarium genus that can cause endoplasmic reticulum (ER) stress and Apoptosis in bovine mammary epithelial cells (MAC-T). Polydatin (PD), a glycoside purified from Polygonum cuspidatum, has antioxidant properties. This study aimed to explore whether PD can alleviate ZEA-induced damage on bovine mammary epithelial cells (MAC-T). We found that incasing the concentration of ZEA (0, 7.5, 15, 30, 60, 90, 120, and 240 μM) gradually decreased the cell viability. PD treatment alone at 5, 10, and 20 μM did not affect cell viability. Follow-up studies then applied 30 μM of ZEA and 5 μM of PD to treat cells; the results showed that the ZEA + PD treatment group effectively reduced cell oxidative damage compared with the ZEA treatment group. The qPCR analysis showed that ZEA treatment significantly up-regulated the expression of ER stress-related genes, relative to the control. However, adding PD significantly down-regulated the expression of ER stress-related genes. The cell apoptosis detection results showed that, compared with the ZEA treatment group, the ZEA + PD treatment group down-regulated the Bax gene and up-regulated the Bcl-2 gene expressions, which reduced the cell apoptosis rate and Caspase-3 activity. Taken together, these results indicate that PD reduces ZEA-induced apoptosis by inhibiting oxidative damage and ER stress.
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spelling pubmed-79152142021-03-01 Polydatin Protects Bovine Mammary Epithelial Cells against Zearalenone-Induced Apoptosis by Inhibiting Oxidative Responses and Endoplasmic Reticulum Stress Fu, Yurong Jin, Yongcheng Shan, Anshan Zhang, Jing Tang, Hongyu Shen, Jinglin Zhou, Changhai Yu, Hao Fang, Hengtong Zhao, Yun Wang, Junxiong Tian, Yue Toxins (Basel) Article Zearalenone (ZEA) is a mycotoxin of the Fusarium genus that can cause endoplasmic reticulum (ER) stress and Apoptosis in bovine mammary epithelial cells (MAC-T). Polydatin (PD), a glycoside purified from Polygonum cuspidatum, has antioxidant properties. This study aimed to explore whether PD can alleviate ZEA-induced damage on bovine mammary epithelial cells (MAC-T). We found that incasing the concentration of ZEA (0, 7.5, 15, 30, 60, 90, 120, and 240 μM) gradually decreased the cell viability. PD treatment alone at 5, 10, and 20 μM did not affect cell viability. Follow-up studies then applied 30 μM of ZEA and 5 μM of PD to treat cells; the results showed that the ZEA + PD treatment group effectively reduced cell oxidative damage compared with the ZEA treatment group. The qPCR analysis showed that ZEA treatment significantly up-regulated the expression of ER stress-related genes, relative to the control. However, adding PD significantly down-regulated the expression of ER stress-related genes. The cell apoptosis detection results showed that, compared with the ZEA treatment group, the ZEA + PD treatment group down-regulated the Bax gene and up-regulated the Bcl-2 gene expressions, which reduced the cell apoptosis rate and Caspase-3 activity. Taken together, these results indicate that PD reduces ZEA-induced apoptosis by inhibiting oxidative damage and ER stress. MDPI 2021-02-05 /pmc/articles/PMC7915214/ /pubmed/33562867 http://dx.doi.org/10.3390/toxins13020121 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Fu, Yurong
Jin, Yongcheng
Shan, Anshan
Zhang, Jing
Tang, Hongyu
Shen, Jinglin
Zhou, Changhai
Yu, Hao
Fang, Hengtong
Zhao, Yun
Wang, Junxiong
Tian, Yue
Polydatin Protects Bovine Mammary Epithelial Cells against Zearalenone-Induced Apoptosis by Inhibiting Oxidative Responses and Endoplasmic Reticulum Stress
title Polydatin Protects Bovine Mammary Epithelial Cells against Zearalenone-Induced Apoptosis by Inhibiting Oxidative Responses and Endoplasmic Reticulum Stress
title_full Polydatin Protects Bovine Mammary Epithelial Cells against Zearalenone-Induced Apoptosis by Inhibiting Oxidative Responses and Endoplasmic Reticulum Stress
title_fullStr Polydatin Protects Bovine Mammary Epithelial Cells against Zearalenone-Induced Apoptosis by Inhibiting Oxidative Responses and Endoplasmic Reticulum Stress
title_full_unstemmed Polydatin Protects Bovine Mammary Epithelial Cells against Zearalenone-Induced Apoptosis by Inhibiting Oxidative Responses and Endoplasmic Reticulum Stress
title_short Polydatin Protects Bovine Mammary Epithelial Cells against Zearalenone-Induced Apoptosis by Inhibiting Oxidative Responses and Endoplasmic Reticulum Stress
title_sort polydatin protects bovine mammary epithelial cells against zearalenone-induced apoptosis by inhibiting oxidative responses and endoplasmic reticulum stress
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7915214/
https://www.ncbi.nlm.nih.gov/pubmed/33562867
http://dx.doi.org/10.3390/toxins13020121
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