线粒体平衡和屏障功能的相互作用在脂聚糖诱导的内皮细胞损伤中的线粒体平衡和屏障功能的相互作用
Weiwei Zhu1, Xiaojing Liu1, Liqing Luo2
1Department of Intensive Care Unit, Binzhou Medical University Hospital, Binzhou, China.
International journal of experimental pathology
|October 13, 2023
概括
线粒体平衡中断会通过增加肝酶 (HPA) 和肌肉素轻链酸化 (p-MLC) 来加剧脂聚糖 (LPS) 诱导的内皮细胞屏障功能障碍. 一个健康的葡萄糖保护了线粒体的功能.
科学领域:
- 内皮细胞生物学 内皮细胞生物学
- 线粒体生理学线粒体生理学
- 细胞屏障功能 细胞屏障功能
背景情况:
- 脂聚糖 (LPS) 触发内皮细胞屏障功能障碍,这是炎症性疾病的关键因素.
- 线粒体平衡在细胞健康和对刺激的反应中起着至关重要的作用.
- 内皮糖核,特别是肝硫酸盐 (HS),对于保持屏障完整性至关重要.
研究的目的:
- 为了研究线粒体平衡对LPS诱导的内皮细胞屏障功能障碍的影响.
- 阐明涉及糖核,肝酶 (HPA) 和紧密结合的潜在机制.
- 为了确定葡萄糖在维护线粒体平衡中所起的保护作用.
主要方法:
- 内皮细胞被用LPS或奥利戈米辛 (线粒体ATP合成酶抑制剂) 治疗.
- 评估了线粒体形态,线粒体反应性氧物种 (mtROS) 和线粒体膜潜力 (ΔΨm).
- 评估了葡萄糖的完整性 (HS脱落),肝酶 (HPA) 水平,紧结 (TJ) 蛋白表达 (occludin,ZO-1),以及肌酸氨酸轻链酸化 (p-MLC).
主要成果:
- 随着肝激酶III治疗,LPS增加了线粒体胀,mtROS和ΔΨm,同时降低了ΔΨm.
- 观察到增加的HS脱落,HPA水平和p-MLC,与奥克卢丁和ZO-1降解相关.
- 肝酶III加剧了线粒体功能障碍和HS脱落,表明了双向关系.
结论:
- 线粒体平衡是LPS诱导的内皮细胞屏障功能障碍的组成部分,由增加的HPA和p-MLC介导.
- 内皮质葡萄糖在维护线粒体平衡中起着保护作用.
- 准线粒体功能和保护糖核糖体可能为内皮屏障保护提供治疗策略.
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