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Chlorogenic acid alleviates deoxynivalenol-induced damage in porcine trophectoderm cells by regulating the PI3K/AKT signaling pathway†

文献类型： 外文期刊

作者： Dai, Chaohui 1 ; Cheng, Jinhua 1 ; Li, Hui 1 ; Zhao, Weimin 1 ; Li, Bixia 1 ; Fu, Yanfeng 1 ; Wang, Xuemin 1 ; Liao, Chao 1 ; Chen, Yanyu 3 ; Yan, Junshu 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Inst Anim Sci, Nanjing 210014, Peoples R China

2.Minist Agr & Rural Affairs, Jiangsu Acad Agr Sci, Key Lab Crop & Livestock Integrat, Nanjing, Peoples R China

3.ProNet Biotech Co Ltd, Nanjing, Peoples R China

关键词： pig; placental trophoblast cells; deoxynivalenol; chlorogenic acid; cell damage

期刊名称：BIOLOGY OF REPRODUCTION （ 影响因子：3.0； 五年影响因子：3.5 ）

ISSN： 0006-3363

年卷期： 2025 年 113 卷 2 期

页码：

收录情况： SCI

摘要： The proliferation and migration of porcine trophectoderm (pTr) cells are crucial processes during the early stages of embryo implantation in sows. The effects of deoxynivalenol (DON) and chlorogenic acid (CGA), a plant-derived compound, on pTr cells are currently unclear. In this study, pTr cells were treated with DON at different times (24, 48, and 72 h) and different concentrations (0.5, 1, and 2 mu g/mL) to construct a pathological model of DON-induced pTr cells by detecting the expression levels of genes related to cell proliferation, migration, and oxidative stress, as well as the cell viability and the cell migration ability. Subsequently, CGA intervention experiments revealed that CGA could promote the proliferation, migration, and antioxidant ability of pTr cells and alleviate the damage induced by DON in pTr cells. Finally, RNA-seq technology combined with experiments illustrated that CGA might alleviate the damage of DON-induced pTr cells by regulating the PI3K/AKT signaling pathway. In conclusion, this study explored the toxicological effect of DON and the alleviation effect of CGA on DON at the pTr cells level, which provided new insights and an experimental basis for using CGA to alleviate the reproductive toxicity induced by DON. Sentence: CGA alleviates DON-induced pTr cells damage.

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