不同氧疗方案对脂多糖诱发的小鼠急性肺损伤的抗炎和保护作用的比较研究。

IF 3 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Medical Gas Research Pub Date : 2025-03-01 Epub Date: 2024-09-25 DOI:10.4103/mgr.MEDGASRES-D-24-00044
Xinhe Wu, Yanan Shao, Yongmei Chen, Wei Zhang, Shirong Dai, Yajun Wu, Xiaoge Jiang, Xinjian Song, Hao Shen
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引用次数: 0

摘要

急性肺损伤后的氧疗可以调节炎症反应,减轻肺组织损伤。然而,急性肺损伤后氧疗的最佳暴露压力、持续时间和频率仍不清楚。在本研究中,ICR 小鼠腹腔注射脂多糖后,1.0 ATA 纯氧和 2.0 ATA 高压氧治疗 1 小时可降低外周血和肺组织中促炎因子(白细胞介素-1beta 和白细胞介素-6)的水平。然而,只有 2.0 ATA 高压氧能提高肺组织中抗炎因子(白细胞介素-10 和精氨酸酶-1)的 mRNA 水平;3.0 ATA 高压氧没有显著影响。我们还观察到,在 2.0 ATA 条件下,单次暴露于高压氧 3 小时的抗炎效果大于单次暴露于高压氧 1 小时的效果。两次暴露于高压氧 1.5 小时的保护作用与一次暴露于高压氧 3 小时的保护作用相似。这些结果表明,在急性肺损伤模型中,高压氧通过调节炎症因子的表达减轻了脂多糖诱导的急性肺损伤,适当增加高压氧暴露的时间和频率对脂多糖诱导的急性肺损伤有更好的组织保护作用。这些结果可指导为急性肺损伤患者制定更有效的氧疗方案。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Comparative study on the anti-inflammatory and protective effects of different oxygen therapy regimens on lipopolysaccharide-induced acute lung injury in mice.

Oxygen therapy after acute lung injury can regulate the inflammatory response and reduce lung tissue injury. However, the optimal exposure pressure, duration, and frequency of oxygen therapy for acute lung injury remain unclear. In the present study, after intraperitoneal injection of lipopolysaccharide in ICR mice, 1.0 atmosphere absolute (ATA) pure oxygen and 2.0 ATA hyperbaric oxygen treatment for 1 hour decreased the levels of proinflammatory factors (interleukin-1beta and interleukin-6) in peripheral blood and lung tissues. However, only 2.0 ATA hyperbaric oxygen increased the mRNA levels of anti-inflammatory factors (interleukin-10 and arginase-1) in lung tissue; 3.0 ATA hyperbaric oxygen treatment had no significant effect. We also observed that at 2.0 ATA, the anti-inflammatory effect of a single exposure to hyperbaric oxygen for 3 hours was greater than that of a single exposure to hyperbaric oxygen for 1 hour. The protective effect of two exposures for 1.5 hours was similar to that of a single exposure for 3 hours. These results suggest that hyperbaric oxygen alleviates lipopolysaccharide-induced acute lung injury by regulating the expression of inflammatory factors in an acute lung injury model and that appropriately increasing the duration and frequency of hyperbaric oxygen exposure has a better tissue-protective effect on lipopolysaccharide-induced acute lung injury. These results could guide the development of more effective oxygen therapy regimens for acute lung injury patients.

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来源期刊
Medical Gas Research
Medical Gas Research MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
5.10
自引率
13.80%
发文量
35
期刊介绍: Medical Gas Research is an open access journal which publishes basic, translational, and clinical research focusing on the neurobiology as well as multidisciplinary aspects of medical gas research and their applications to related disorders. The journal covers all areas of medical gas research, but also has several special sections. Authors can submit directly to these sections, whose peer-review process is overseen by our distinguished Section Editors: Inert gases - Edited by Xuejun Sun and Mark Coburn, Gasotransmitters - Edited by Atsunori Nakao and John Calvert, Oxygen and diving medicine - Edited by Daniel Rossignol and Ke Jian Liu, Anesthetic gases - Edited by Richard Applegate and Zhongcong Xie, Medical gas in other fields of biology - Edited by John Zhang. Medical gas is a large family including oxygen, hydrogen, carbon monoxide, carbon dioxide, nitrogen, xenon, hydrogen sulfide, nitrous oxide, carbon disulfide, argon, helium and other noble gases. These medical gases are used in multiple fields of clinical practice and basic science research including anesthesiology, hyperbaric oxygen medicine, diving medicine, internal medicine, emergency medicine, surgery, and many basic sciences disciplines such as physiology, pharmacology, biochemistry, microbiology and neurosciences. Due to the unique nature of medical gas practice, Medical Gas Research will serve as an information platform for educational and technological advances in the field of medical gas.
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