纳米颗粒通过调节IPEC-J2细胞内质网膜应激来缓解脱氧尼瓦伦醇诱导的肠上皮屏障功能障碍
Xiaofan Song1, Lei Qiao1, Xina Dou1
1The Key Laboratory for Space Bioscience and Biotechnology, School of Life Sciences, Northwestern Polytechnical University, Xi'an, Shaanxi 710072, China.
Toxicology
|July 13, 2023
概括
纳米颗粒 (SeNPs) 通过PERK通路减轻氧化应激和内分泌网膜应激,保护免受脱氧 (DON) 诱导的肠壁损伤. 这为水产养殖中DON污染提供了潜在的解决方案.
科学领域:
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
- 纳米技术 纳米技术
背景情况:
- 肠上皮屏障对健康至关重要,但容易受到除氧烯 (DON) 等真菌毒素的损害.
- 多是谷物中普遍存在的污染物,对人类和动物健康构成重大风险.
- 纳米颗粒 (SeNPs) 显示出有前途的保护剂对毒素诱导的细胞损伤.
研究的目的:
- 研究Lactobacillus casei合成的纳米颗粒 (SeNPs) 对DON诱导的肠上皮屏障功能障碍的保护作用.
- 阐明PERK介导的内质网膜应激 (ERS) 信号通路在SeNPs对DON的保护机制中的作用.
主要方法:
- IPEC-J2细胞暴露于DON和/或SeNPs,治疗包括PERK通路激动剂和抑制剂.
- 评估的参数包括体电阻 (TEER),紧结蛋白表达,活性氧物种 (ROS) 含量,抗氧化能力和内细胞网膜 (ER) 形态.
- 通过测量p-PERK水平,评估了与ERS相关的PERK通路的激活.
主要成果:
- 暴露于DON显著增加了肠上皮的透性,减少了紧结蛋白,增加了ROS,降低了抗氧化能力,并诱导了ER结构损伤和PERK通路激活.
- 治疗SeNPs缓解了DON诱导的氧化应激,ER损伤和PERK通路激活,从而改善了肠道屏障功能.
- PERK通路调节证实了它的参与;PERK抑制剂模仿了SeNPs对p-PERK表达的保护作用.
结论:
- 纳米颗粒 (SeNPs) 有效地减轻IPEC-J2细胞中脱氧尼瓦 (DON) 诱导的肠表皮屏障功能障碍.
- SeNPs的保护机制与抑制内细胞网膜与压力相关的PERK信号通路密切相关.
- 在水产养殖行业中,SeNPs代表了管理DON污染的潜在策略.
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