肉酸通过激活Nrf2/HO-1通路来减轻呼吸器诱导的隔膜功能障碍
Zilin Liu1, Qian Yu2, Xianlong Zhou2
1Emergency Center, Zhongnan Hospital of Wuhan University, 430071 Wuhan, Hubei, China; Hubei Provincial Clinical Research Center for Emergency and Resuscitation, Zhongnan Hospital of Wuhan University, 430071 Wuhan, China; Department of Spine Surgery and Musculoskeletal Tumor, Zhongnan Hospital of Wuhan University, 169 Donghu Street, Wuchang District, Wuhan 430071, Hubei, China.
International immunopharmacology
|November 23, 2025
概括
肉酸 (CA) 通过减少肌肉缩和亡,防止呼吸器诱导的隔膜功能障碍 (VIDD). 这种天然化合物在预防和治疗VIDD方面表现有前途,改善腹膜功能.
科学领域:
- 生物化学 生化学
- 细胞生物学 细胞生物学
- 身体生理学 身体生理学
背景情况:
- 长时间的机械通风 (MV) 可以导致呼吸器诱导的隔膜功能障碍 (VIDD),其特点是肌肉缩,收缩能力降低和耐力受损.
- VIDD的关键机制包括线粒体功能障碍和隔膜肌细胞中的亡.
- 炭酸 (CA) 是一种天然的抗氧化和抗炎化合物,具有潜在的治疗益处,但其在VIDD中的作用尚未被探索.
研究的目的:
- 调查卡诺西克酸 (CA) 对呼吸机诱导的隔膜功能障碍 (VIDD) 的保护作用.
- 阐明CA在预防隔膜损伤和缩方面的作用的基本机制.
主要方法:
- 建立了体内 (小鼠) 和体外 (C2C12神经管) 的VIDD和肌肉缩模型.
- 给模型受试者注射CA并评估隔膜功能,氧化应激,缩标志物和亡,使用超声波,西部涂抹和流动细胞计等技术.
- 使用JC-1染色和传输电子显微镜评估线粒体形态和功能.
主要成果:
- 在MV和甲 (DXMS) 暴露下,CA治疗减轻了腹膜肌细胞的氧化应激,缩和亡.
- 它提高了Nrf2/HO-1通路的调节,改善了线粒体功能,并减少了氧化应激标志物 (ROS,MDA).
- CA抑制了亲亡的因素 (Bax,Caspase-3/9) 和增加了抗亡的因素 (Bcl-2),保持了肌肉功能.
结论:
- 肉酸 (CA) 激活Nrf2/HO-1通路,减轻线粒体损伤和肌细胞的亡.
- CA有效地减轻肌肉缩,并保持隔膜生理功能.
- CA显示出作为一种新型治疗剂的潜力,用于预防和治疗呼吸机诱导的隔膜功能障碍 (VIDD).
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