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Tannic acid repair of zearalenone-induced damage by regulating the death receptor and mitochondrial apoptosis signaling pathway in mice
Environmental Pollution ( IF 7.6 ) Pub Date : 2021-06-09 , DOI: 10.1016/j.envpol.2021.117557
Jing Wu 1 , Jiayan Li 1 , Yanwei Liu 1 , Xinxin Liao 1 , Dongyi Wu 1 , Yunqin Chen 1 , Zengenni Liang 2 , Zhihang Yuan 1 , Rongfang Li 1 , Jine Yi 1 , Lixin Wen 3
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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.

中文翻译:

单宁酸通过调节死亡受体和线粒体凋亡信号通路修复玉米赤霉烯酮引起的损伤

玉米赤霉烯酮(ZEA)是镰刀菌菌株产生的雌激素毒素,广泛存在于农作物中,危害动物的生殖系统。单宁酸(TA)是一种天然多酚物质,广泛存在于植物的根、茎、叶中,具有特殊的药理活性。本研究旨在探讨TA对ZEA诱导的小鼠卵巢损伤的治疗作用并探讨其分子机制。将90只健康昆明雌性小鼠分为6个相等的组。除对照组外,所有组每天口服 ZEA [10 mg/kg 体重 (bw)],持续 7 天,以诱导生殖系统损伤。有些组还服用 TA(50、100 和 200 毫克/体重)7 天。 24小时后将小鼠安乐死以收集血清和卵巢。 TA可以有效缓解ZEA引起的卵巢充血和发红现象,并增加健康生长的卵泡数量。此外,TA还能有效降低卵巢中雌激素含量以及MDA和ROS水平。还能减少卵巢细胞的凋亡,降低雌激素受体Fas、Fasl、caspase-3、caspase-8、caspase-9、Bax的蛋白表达,增加Bcl-2的蛋白表达。我们的研究表明,TA 减少了 ZEA 引起的强雌激素和氧化损伤,这些治疗作用可能部分是由死亡受体和线粒体凋亡信号通路介导的。
更新日期:2021-06-09
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