电针通过调节Nrf2/HO-1通路来减轻风扇引起的肺损伤
Jiansheng Luo1, Ruyu Yan1, Lingling Ding1
1Department of Anesthesiology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
The Journal of surgical research
|December 31, 2023
概括
电针 (EA) 通过减少炎症和氧化应激减轻呼吸器诱导的肺损伤 (VILI). 这项研究表明,EA激活了Nrf2/HO-1通路,抑制NLRP3炎症酶,以保护肺部.
科学领域:
- 肺部病理学 肺部病理学
- 综合医学是一个整体的医学.
- 分子生物学分子生物学
背景情况:
- 呼吸机引起的肺损伤 (VILI) 是机械呼吸的常见并发症.
- 电针 (EA) 显示出显著的抗炎性质.
- 研究EA对VILI及其潜在机制的治疗潜力至关重要.
研究的目的:
- 评估电针 (EA) 在缓解呼吸机诱导的肺损伤 (VILI) 的有效性.
- 阐明EA通过哪些分子机制来发挥其对VILI的保护作用.
主要方法:
- 雄性C57BL/6小鼠接受了高潮量通风,以诱导VILI.
- 小鼠接受了包括EA,无点EA或EA与原氨酸结合的治疗.
- 评估了肺损伤,炎症,氧化应激和分子通路的关键指标.
主要成果:
- 治疗EA显著改善了氧化 (PaO2) 并减少了肺损伤标志物 (肺损伤得分,湿/干重量比,BALF蛋白).
- EA降低了促炎性细胞因子 (IL-1β,IL-6,TNF-α) 和氧化应激标志物 (甲).
- EA上调调节了Nrf2/HO-1表达,并降低了p-NF-κB p65,NLRP3,Caspase-1和ASC的表达;无点EA和原氨酸逆转了这些效应.
结论:
- 电针 (EA) 有效地缓解了呼吸机诱导的肺损伤 (VILI).
- 通过激活Nrf2/HO-1通路,EA通过抑制NLRP3炎症酶来发挥其保护作用.
- 这些发现突出了EA作为VILI的潜在治疗策略.
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