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Multi-omics analysis reveals the molecular mechanism of silibinin rescue the toxic effects of butyl benzyl phthalate on porcine preimplantation embryos

文献类型： 外文期刊

作者： Li, Yu 1 ; Huang, Guangjun 1 ; Li, Na 1 ; Zhang, Zihao 1 ; Zhang, Hanwen 1 ; Gao, Qian 2 ; Cui, Zhaokang 3 ; Jiang, Yi 4 ; Miao, Yilong 1 ;

作者机构： 1.Nanjing Agr Univ, Coll Anim Sci & Technol, Nanjing 210095, Peoples R China

2.Nanjing Agr Univ, Coll Vet Med, Nanjing 210095, Peoples R China

3.Jiangsu Acad Agr Sci, Institue Anim Sci, Nanjing 210014, Peoples R China

4.Hebei Leren Biotechnol Co LTD, Shijiazhuang 050000, Peoples R China

关键词： Embryo development; Oxidative stress; BBP; Silibinin

期刊名称：JOURNAL OF HAZARDOUS MATERIALS （ 影响因子：11.3； 五年影响因子：12.4 ）

ISSN： 0304-3894

年卷期： 2025 年 495 卷

页码：

收录情况： SCI

摘要： BBP exposure induces oxidative stress in preimplantation embryos, elevating reactive oxygen species (ROS) and impairing mitochondrial function via NDUFA11 dysfunction (mitochondrial complex I). This disrupts ATP synthesis and mitochondrial membrane potential, exacerbating oxidative damage. Silibinin supplementation rescues BBP-induced embryotoxicity by restoring NDUFA11 function, normalizing mitochondrial activity, and enhancing developmental competence. Our findings delineate BBP's embryotoxic mechanisms and identify silibinin as a therapeutic candidate for counteracting environmental EDC-associated reproductive risks. Journal of Hazardous Materials 495 (2025) 138900 experimental results indicate that BBP exposure significantly inhibits the development process of early embryos, reducing the proportion of embryos reaching key formation stages. Through transcriptomic and metabolomic analyses, we found that BBP exposure leads to marked changes in gene expression and metabolite levels associated with mitochondrial function and protein translation, accompanied by structural damage to the endoplasmic reticulum and Golgi apparatus. The study also reveals that BBP may disrupt mitochondrial function through interaction with the mitochondrial membrane protein NDUFA11, thereby inducing oxidative stress and apoptosis. The innovation of this research lies in proposing that silibinin, a natural antioxidant, can effectively alleviate BBP-induced developmental disorders in embryos, offering a new strategy for protecting maternal reproductive health. This work not only provides a scientific basis for understanding the embryotoxicity of BBP but also offers important insights for the health risk assessment and prevention of environmental endocrine disruptors.

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