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Maintaining the Mitochondrial Quality Control System Was a Key Event of Tanshinone IIA against Deoxynivalenol-Induced Intestinal Toxicity

文献类型: 外文期刊

作者: Zhang, Cong 1 ; Wang, Youshuang 1 ; Zhang, Xinyu 1 ; Zhang, Kefei 1 ; Chen, Fengjuan 1 ; Fan, Jiayan 1 ; Wang, Xuebing 1 ; Yang, Xu 1 ;

作者机构: 1.Henan Acad Agr Sci, Coll Vet Med, Zhengzhou 450002, Peoples R China

2.Minist Agr & Rural Affairs, Key Lab Qual & Safety Control Poultry Prod, Zhengzhou 450046, Peoples R China

关键词: Tanshinone IIA; deoxynivalenol; mitochondrial quality control; IPEC-J2 cells

期刊名称:ANTIOXIDANTS ( 影响因子:7.0; 五年影响因子:7.3 )

ISSN:

年卷期: 2024 年 13 卷 1 期

页码:

收录情况: SCI

摘要: Deoxynivalenol (DON) is the one of the most common mycotoxins, widely detected in various original foods and processed foods. Tanshinone IIA (Tan IIA) is a fat-soluble diterpene quinone extracted from Salvia miltiorrhiza Bunge, which has multi-biological functions and pharmacological effects. However, whether Tan IIA has a protective effect against DON-induced intestinal toxicity is unknown. In this study, the results showed Tan IIA treatment could attenuate DON-induced IPEC-J2 cell death. DON increased oxidation product accumulation, decreased antioxidant ability and disrupted barrier function, while Tan IIA reversed DON-induced barrier function impairment and oxidative stress. Furthermore, Tan IIA dramatically improved mitochondrial function via mitochondrial quality control. Tan IIA could upregulate mitochondrial biogenesis and mitochondrial fusion as well as downregulate mitochondrial fission and mitochondrial unfolded protein response. In addition, Tan IIA significantly attenuated mitophagy caused by DON. Collectively, Tan IIA presented a potential protective effect against DON toxicity and the underlying mechanisms were involved in mitochondrial quality control-mediated mitophagy.

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