在LPS诱导的心脏毒性中,FOXO1调节NLRP3炎症酶蛋白
Hui Zhao1, Lingcun Qin2, Ruyi Wang3
1Department of Cardiology, Tianjin Fifth Central Hospital Tianjin, China.
American journal of translational research
|September 11, 2023
概括
叉头盒蛋白O1 (FOXO1) 通过减少炎症和细胞死亡来保护免受脂聚糖 (LPS) 引起的心脏损伤. 抑制FOXO1通过NLRP3炎症酶途径恶化LPS心脏毒性.
科学领域:
- 心血管生物学 心血管生物学
- 分子医学是分子医学.
- 细胞毒理学细胞毒理学
背景情况:
- 叉头盒蛋白O1 (FOXO1) 在心血管过程中起作用.
- FOXO1对脂聚糖 (LPS) 诱导的心脏毒性的影响尚不清楚.
研究的目的:
- 调查FOXO1在LPS引起的心脏毒性的作用.
- 探索FOXO1对LPS诱导的心肌细胞损伤的影响的潜在机制.
主要方法:
- 使用的H9c2细胞暴露于LPS.
- 通过腺相关病毒和siRNA操纵FOXO1表达.
- 评估了细胞活力,细胞亡,炎症性细胞因子 (IL-1β,IL-18,TNF-α) 和活性氧物种 (ROS).
- 检查了NLRP3炎症酶通路的参与.
主要成果:
- 在剂量和时间的依赖下,LPS降低了FOXO1的表达.
- 过度表达FOXO1减弱了LPS诱导的亡,氧化应激和炎症.
- FOXO1抑制加剧了LPS诱导的心肌细胞损伤.
- FOXO1通过降低NLRP3.3的调节来调节LPS诱导的心肌损伤.
结论:
- 过度表达FOXO1可以减轻LPS诱导的亡,ROS生成和炎症.
- 抑制FOXO1通过NLRP3炎症酶途径加剧LPS诱导的心肌细胞损伤.
- FOXO1是一种保护因子,可以防止LPS引起的心脏毒性.
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