Selenium nanoparticles alleviate deoxynivalenol-induced intestinal epithelial barrier dysfunction by regulating endoplasmic reticulum stress in IPEC-J2 cells

被引:9
作者
Song, Xiaofan [1 ]
Qiao, Lei [1 ]
Dou, Xina [1 ]
Chang, Jiajing [1 ]
Zhang, Yafeng [2 ]
Xu, Chunlan [1 ,3 ]
机构
[1] Northwestern Polytech Univ, Sch Life Sci, Key Lab Space Biosci & Biotechnol, Xian 710072, Shaanxi, Peoples R China
[2] Xian Inst Food & Drug, 889 Cangtai West Rd, Xian 710700, Shaanxi, Peoples R China
[3] Northwestern Polytech Univ, Sch Life Sci, 127 Youyixi Rd Xian, Xian 710072, Shaanxi, Peoples R China
基金
中国国家自然科学基金;
关键词
Selenium nanoparticles; Deoxynivalenol; Endoplasmic reticulum stress; Intestinal barrier function; OXIDATIVE STRESS; AFLATOXIN; APOPTOSIS; HEALTH;
D O I
10.1016/j.tox.2023.153593
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The intestinal epithelial barrier plays a crucial role in maintaining human and animal health. Deoxynivalenol (DON) is a mycotoxin that contaminates cereal-based foods worldwide, which is a serious threat to human and animal health. This study was aimed to investigate the protective effect of selenium nanoparticles (SeNPs) synthesized by Lactobacillus casei ATCC 393 against DON-induced intestinal epithelial barrier dysfunction and its relationship with PERK-mediated signaling pathway. IPEC-J2 cells were randomly assigned to four groups: Con (vehicle), DON (0.6 mu g DON/mL, 48 h), SeNPs+DON (8 mu g Se/mL, 24 h; 0.6 & mu;g DON/mL, 48 h) and SeNPs (8 mu g Se/mL, 24 h). Compared with Con group, the transepithelial electrical resistance (TEER) and the tight junction proteins expression of IPEC-J2 cells exposed to DON was increased and decreased, respectively. In addition, DON exposure led to increased ROS content, decreased antioxidant capacity, structural damage of endoplasmic reticulum (ER), and activation of endoplasmic reticulum stress (ERS)-related protein kinase R-like endoplasmic reticulum kinase (PERK) pathway in IPEC-J2. Compared with SeNPs+DON group, SeNPs alleviated oxidative stress, ER structure damage and PERK pathway activation and the increase of intestinal epithelial permeability of IPEC-J2 cells exposed to DON. PERK agonist (CCT020312) and inhibitor (GSK2656157) treatments were performed to identify the role of PERK signaling pathway in the regulatory effects of SeNPs on DON-induced intestinal epithelial barrier dysfunction. Compared with SeNPs+DON group, PERK agonist increased the expression levels of p-PERK. PERK inhibitor exerted a similar inhibitory effect to SeNPs on the p-PERK expression. In conclusion, SeNPs effectively alleviate DON-induced intestinal epithelial barrier dysfunction in IPEC-J2 cells, which are closely associated with ERS-related PERK signaling pathway. This will provide a potential solution for prevention and control of DON in the aquaculture industry.
引用
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页数:11
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