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Glycyrrhizin Alleviates the Damage Caused by Zearalenone and Protects the Glandular Stomach of Chickens

Journal 2025 · IF 2.7 · 15(4): 489 · 发表于 2025 年 2 月 9 日
作者: Tong Sun,Fuhan Wang,Man Qian,Jingjing Wang,Mengyao Guo
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摘要

Simple SummaryZearalenone (ZEA) is a mycotoxin that widely contaminates feed. Glycyrrhizin acid (GA) is a traditional Chinese medicine extract of licorice. This study found that GA could alleviate the damage to chicken glands and stomachs caused by ZEA in vivo, reduce the levels of oxidative stress in the body, and reduce the number of instances of apoptosis and programmed necrosis. GA may inhibit apoptosis and programmed necrosis mediated by inflammation through the NFκB pathway and protect the glandular gastric tissue. These results provide indirection for toxicological studies of ZEA and therapeutic effects of GA and help further explore the toxic effects of mycotoxins on the digestive tract.Zearalenone (ZEA) is a kind of mycotoxin that widely contaminates food and feed and poses a threat to poultry farming. As a natural extract, glycyrrhizin acid (GA) has antioxidant, antibacterial, and anti-inflammatory effects. Although studies have revealed the toxic effects of ZEA on the liver, the mechanism by which GA reduces ZEA’s toxic protective glandular stomach remains unclear. In order to study the therapeutic effect of GA on tissue damage caused by ZEA, we conducted in vivo and in vitro experiments to compare the expression of inflammation, oxidative stress, apoptosis, and necrosis. The results showed that ZEA can induce inflammation in tissues and cells, inducing apoptosis and necrosis. In addition, GA can alleviate the toxic effects caused by ZEA and protect cells. Dietary GA significantly increased the antioxidant capacity of glandulae and inhibited the overexpression of NFκB/IκB-α and its mediated inflammatory response. Moreover, GA decreased the expression of pro-apoptotic factors and necrosis factors, thereby alleviating apoptosis and necrosis of chicken glandular stomach cells. At present, the mechanism of ZEA damage to livers and lungs has been confirmed by studies. However, there have been no studies on GA alleviating the damage caused by ZEA to the glandular stomach. Therefore, the purpose of this study was to explore the mechanism of GA alleviating the damage caused by ZEA in the glandular stomach through in vivo and in vitro experimental comparison. The results may provide some reference for the solution of feed contamination.

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