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寒冷的压力会通过通过p38 MAPK/Drp1通路诱导铁亡导致肝损伤

Yujie Huang¹, Kun Xiong¹, Aiping Wang¹

¹Department of Cold Environmental Medicine, College of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Shapingba District, Chongqing, 400038, PR China; Key Laboratory of Extreme Environmental Medicine, Ministry of Education of China, Chongqing, PR China; Key Laboratory of High Altitude Medicine, PLA, Chongqing, PR China.

|August 2, 2023

概括

极端寒冷的暴露会通过诱导细胞死亡途径铁亡引起肝损伤. 抑制铁亡,特别是通过p38 MAPK/Drp1通路,可以保护免受寒冷压力诱导的肝损伤.

科学领域:

细胞生物学细胞生物学
毒理学毒理学毒理学
身体生理学身体生理学

背景情况:

暴露于急性极度寒冷会给健康带来重大风险,包括低温症.
肝脏在寒冷适应期间的新陈代谢和热生成中发挥着至关重要的作用.
造成寒冷压力引起的肝损伤背后的机制尚未完全理解.

研究的目的:

为了研究铁死在由寒冷压力引起的肝损伤中的作用.
阐明潜在的分子机制,包括p38 MAPK/Drp1通路.

主要方法:

鼠被暴露在-10°C下8小时.
他们使用了铁灭抑制剂 (liproxstatin-1),p38 MAPK 抑制剂 (SB203580) 和 Drp1 抑制剂 (Mdivi-1).
评估了铁亡指标,肝功能标志物 (ALT,AST),肝病理和线粒体分裂.

主要成果:

暴露于寒冷导致铁亡和肝损伤,由高ALT/AST和病理变化证明.
利普洛克斯塔丁-1治疗减轻了感冒引起的肝损伤和铁亡.
抑制p38 MAPK或Drp1 (Mdivi-1) 抑制了线粒体分裂和铁亡,缓解了肝损伤.

结论:

寒冷压力会导致肝损伤,部分原因是铁亡.
在p38 MAPK/Drp1通路中介于感冒诱导的铁和随后的肝损伤.
向ferroptosis为感冒压力诱导的肝损伤提供了一个潜在的治疗策略.

关键词:

寒冷的压力是冷的压力.DRP1 是一个DRP1 铁化是铁化的一种.肝脏损伤肝脏损伤在P38 MAPKK中使用.

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