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Tannic acid repair of zearalenone-induced damage by regulating the death receptor and mitochondrial apoptosis signaling pathway in mice

文献类型： 外文期刊

作者： Wu, Jing 1 ; Li, Jiayan 1 ; Liu, Yanwei 1 ; Liao, Xinxin 1 ; Wu, Dongyi 1 ; Chen, Yunqin 1 ; Liang, Zengenni 4 ; Yuan, Zh 1 ;

作者机构： 1.Hunan Agr Univ, Hunan Engn Res Ctr Livestock & Poultry Hlth Care, Changsha 410128, Peoples R China

2.Hunan Agr Univ, Coll Vet Med, Changsha 410128, Peoples R China

3.Hunan Coinnovat Ctr Anim Prod Safety, Changsha 410128, Peoples R China

4.Hunan Acad Agr Sci, Hunan Agr Prod Proc Inst, Changsha 410125, Peoples R China

关键词： Zearalenone; Oxidative stress; Apoptosis; Death receptor signaling pathway; Mitochondrial apoptosis signaling pathway

期刊名称：ENVIRONMENTAL POLLUTION （ 影响因子：8.071； 五年影响因子：8.35 ）

ISSN： 0269-7491

年卷期： 2021 年 287 卷

页码：

收录情况： SCI

摘要： Zearalenone (ZEA) is an estrogenic toxin produced by Fusarium strains, that is widely present in crops, and endangers the reproductive system of animals. Tannic acid (TA) is a natural polyphenolic substance that is widespread in the roots, stems, and leaves of plants, and has special pharmacological activity. This study was designed to investigate the therapeutic effect of TA on ZEA-induced ovarian damage in mice and to explore the molecular mechanism involved. Ninety healthy Kunming female mice were divided into six equal groups. All the groups but the control group were administered daily with ZEA [10 mg/kg body weight (bw)] orally, for 7 days, to induce damage to the reproductive system. Some groups were also administered with TA (50, 100, and 200 mg/bw) for 7 days. Mice were euthanized 24 h later to allow for collection of serum and ovaries. TA can effectively alleviate the appearance of congestion and redness of the ovary, caused by ZEA, and increase the number of healthy growing follicles. Moreover, the estrogen content and the levels of MDA and ROS in the ovaries can be effectively reduced by TA. It can also reduce the apoptosis of ovarian cells, decreases the protein expression of the estrogen receptor, Fas, Fasl, caspase-3, caspase-8, caspase-9, and Bax, and increases the protein expression of Bcl-2. Our study indicates that TA reduces the strong estrogen and oxidative damage induced by ZEA, and these therapeutic effects may be partially mediated by the death receptor and mitochondrial apoptosis signaling pathway.

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