热空气通过ERK1/2信号介导的铁灭损伤人类气膜上皮细胞
Ruihan Liu1, Zhihui Wang1, Qing Luo1
1Key Laboratory of Biorheological Science and Technology, College of Bioengineering, Chongqing University, Chongqing, 400030, China.
Journal of thermal biology
|February 2, 2025
概括
在50°C的热应激 (HS) 会导致铁亡和膜上皮细胞的损伤. 这一过程涉及细胞外信号调节激酶1/2 (ERK1/2) 信号,为热引起的肺损伤提供了潜在的治疗标.
科学领域:
- 肺部医学 肺部医学
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
背景情况:
- 吸入热空气/有毒气体造成的肺损伤是一个关键问题.
- 在膜上皮细胞中热应激 (HS) 的分子机制尚不清楚.
研究的目的:
- 研究人类膜上皮细胞 (BEAS-2B) 中HS诱导的损伤的分子机制.
- 探索铁和ERK1/2信号在HS引起的肺损伤中的作用.
主要方法:
- 使用细胞热加载装置将BEAS-2B细胞暴露在50°C的高温环境中.
- 评估了细胞损伤,脂质过氧化,活性氧物种 (ROS) 和关键的铁亡标志物 (FTH1,GPX4,SLC7A11).
- 研究了ferroptosis抑制剂 (Fer-1) 和ERK1/2抑制剂 (U0126) 对HS诱导的细胞损伤的影响.
主要成果:
- 在BEAS-2B细胞中,HS诱导了显著的铁亡和损伤,由增加的脂质过氧化和ROS证明,并降低了FTH1,GPX4和SLC7A11.
- 铁素-1 (Fer-1) 有效抑制HS诱导的铁和细胞损伤.
- HS激活了ERK1/2信号,并阻断了ERK1/2与U0126的酸化,抑制了HS诱导的铁和损伤.
结论:
- 热应激通过ERK1/2信号介导的铁灭损伤膜上皮细胞.
- 针对ERK1/2信号提供了一种新的治疗策略,用于治疗热应激引起的吸入性肺损伤.
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