阿弗拉托克素B1通过AMPK/NLRP3途径扰乱线粒体动力学,促进IPEC-J2细胞中的灭
Jiayi Ding1, Xinyi Cheng1, Chun Zeng1
1Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang, Jiangxi 330045, P. R. China.
Journal of agricultural and food chemistry
|December 4, 2024
概括
非洲毒素B1 (AFB1) 通过激活AMPK/NLRP3通路,导致热和线粒体功能障碍,导致肠道损伤. 抑制这些通路可以保护肠道细胞免受AFB1损伤.
科学领域:
- 胃肠病学 胃肠病学
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 甲毒素B1 (AFB1) 是一种强大的真菌毒素,对肠道健康构成重大风险.
- 导致AFB1引起的肠损伤的确切机制尚未完全阐明.
研究的目的:
- 为了研究AMP激活蛋白激酶 (AMPK) 介导的热死在AFB1诱导的肠损伤中的作用.
- 探索AFB1对线粒体动态及其与细胞损伤的联系的影响.
主要方法:
- 使用实验室模型 (IPEC-J2细胞) 来研究AFB1的影响.
- 评估了烧亡标志物 (LDH,IL-1β) 和NLRP3通路的激活.
- 通过分析动胺-1-样蛋白1 (Drp1) 表达的方法,检查了线粒体动态.
- 研究了NLRP3和AMPK途径抑制剂 (MCC950,化合物C) 的作用.
主要成果:
- AFB1诱导细胞膜损伤,释放LDH和IL-1β,表明热.
- AFB1激活了NLRP3炎症酶途径,增加了热的发生率.
- AFB1通过激活AMPK通路和调高Drp1.1来破坏线粒体动力学.
- 抑制NLRP3和AMPK通路显著降低了AFB1诱导的肠细胞损伤.
结论:
- AFB1通过AMPK/NLRP3通路破坏线粒体动力学来促进肠道细胞烧灭.
- 针对AMPK和NLRP3通路提供了针对AFB1诱导的肠损伤的潜在治疗策略.
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