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 genus that can cause endoplasmic reticulum (ER) stress and Apoptosis in bovine mammary epithelial cells (MAC-T). Polydatin (PD), a glycoside purified from has antioxidant properties. This study aimed to explore whether PD can alleviate ZEA-induced damage on bo...
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Published in | Toxins Vol. 13; no. 2; p. 121 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
MDPI
05.02.2021
MDPI AG |
Subjects | |
Online Access | Get full text |
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Summary: | Zearalenone (ZEA) is a mycotoxin of the
genus that can cause endoplasmic reticulum (ER) stress and Apoptosis in bovine mammary epithelial cells (MAC-T). Polydatin (PD), a glycoside purified from
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
gene and up-regulated the
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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 YuRong Fu and Yongcheng Jin should be considered joint first author. |
ISSN: | 2072-6651 2072-6651 |
DOI: | 10.3390/toxins13020121 |