铁素-1通过抑制铁灭菌来缓解呼吸器诱导的肺损伤
Maoyao Ling1, Liu Ye1, Qi Zeng2
1Department of Anesthesiology, Guangxi Medical University Cancer Hospital, Nanning, China; Guangxi Engineering Research Center for Tissue & Organ Injury and Repair Medicine, Nanning, China; Guangxi Health Commission Key Laboratory of Basic Science and Prevention of Perioperative Organ Disfunction, Nanning, China; Guangxi Clinical Research Center for Anesthesiology, Nanning, China.
International immunopharmacology
|May 27, 2023
概括
呼吸器诱导的肺损伤 (VILI) 涉及炎症;这项研究揭示了细胞死亡形式铁亡,有助于VILI. 通过ferrostain-1抑制铁亡,保护小鼠和细胞免受肺损伤.
科学领域:
- 肺部医学 肺部医学
- 细胞生物学 细胞生物学
- 炎症研究 炎症研究
背景情况:
- 呼吸机引起的肺损伤 (VILI) 是一种常见的机械通风并发症.
- 驱动VILI的精确炎症机制仍然不完全理解.
- 铁亡是一种受调节的细胞死亡途径,释放与损伤相关的分子模式 (DAMPs),可以加剧炎症.
研究的目的:
- 调查铁灭菌在VILI的病变发生中的作用.
- 在VILI模型中评估抑制ferroptosis的治疗潜力.
主要方法:
- 已建立的小鼠和肺上皮细胞模型的VILI由高潮量 (HTV) 和循环拉伸 (CS) 诱导.
- 在VILI模型中给药ferrostain-1,一种铁灭抑制剂.
- 在体内和体外评估肺损伤,炎症和与铁亡相关的标志物 (包括SLC7A11/GPX4轴).
主要成果:
- 在小鼠中,HTV暴露导致肺胀,炎症和铁灭激活的增加.
- 在VILI小鼠中,Ferrostain-1治疗显著降低了组织学肺损伤和炎症.
- 费罗斯坦-1缓解了CS诱导的肺上皮细胞损伤,并恢复了SLC7A11/GPX4轴的功能.
结论:
- 铁死在VILI的发展中起着重要作用.
- 使用ferrostain-1抑制ferroptosis证明了缓解VILI的治疗潜力.
- 向铁亡途径,特别是SLC7A11/GPX4轴,为VILI治疗提供了一种新的策略.
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