通过自性-CTSB-NLRP3通路诱导的乙酸诱导的肝细胞烧灭
Jing Lu1, Ziheng Chen1, Xiujuan Bu1
1College of Food Science and Engineering, Jilin University, Changchun, Jilin, 130062, People's Republic of China.
概括
乙酸 (EA) 是加工食品中的一种转脂肪酸,会触发肝细胞死亡,称为热亡. 这通过一种涉及自,甲素B和NLRP3炎症酶的途径发生,导致肝损伤.
科学领域:
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
- 生物化学 生物化学
背景情况:
- 像酸 (EA) 一样,反式脂肪酸 (TFAs) 在加工食品中普遍存在.
- 热症是一种促炎性编程细胞死亡途径,涉及到组织损伤.
- EA对热的特定影响及其潜在机制在很大程度上仍未被探索.
研究的目的:
- 为了研究乙烯酸 (EA) 对肝细胞中热的作用.
- 阐明EA诱导热的分子机制.
- 探索自和溶酶体通路在EA介导的灭中的作用.
主要方法:
- 暴露小鼠和HepG2细胞以乙烯酸 (EA).
- 评估热致死标记物 (GSDMD-N,卡斯帕斯1,IL-18,IL-1β).
- 调查自,溶酶体膜通透 (LMP),甲素B (CTSB) 泄漏,以及NLRP3炎症酶激活.
- 使用3-MA的自的药理抑制.
主要成果:
- 在体内和体外,EA暴露引起了显著的肝损伤和肝细胞灭.
- 由EA诱导的热死取决于由cathepsin B (CTSB) 介导的NLRP3炎症酶激活.
- EA促进了肝细胞自,导致溶酶体膜通透 (LMP) 和CTSB释放.
- 通过减少CTSB泄漏和NLRP3炎症酶激活,抑制自减弱EA诱导的火灭菌.
结论:
- 乙烯酸 (EA) 通过自性-CTSB-NLRP3炎症酶途径诱导肝细胞烧灭.
- 这项研究揭示了EA毒性影响肝脏健康的新型机制.
- 准自-NLRP3炎症酶轴可能提供针对EA诱导的肝损伤的治疗策略.
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