Hydrogen‐rich and hyperoxygenate saline inhibits lipopolysaccharide‐induced lung injury through mediating NF‐κB/NLRP3 signaling pathway in C57BL/6 mice

支气管肺泡灌洗 活性氧 脂多糖 缺氧(环境) 化学 细胞凋亡 药理学 低氧血症 生理盐水 腹腔注射 医学 免疫学 氧气 生物化学 麻醉 内科学 有机化学
作者
Yingying Fan,Jian Wang,Zhihui Feng,Ke Cao,Jiankang Liu,Hao Xu
出处
期刊:Environmental Toxicology [Wiley]
卷期号:37 (7): 1575-1586 被引量:12
标识
DOI:10.1002/tox.23507
摘要

Abstract Background Background: Acute lung injury (ALI) is one kind of frequently occurred emergency in Intensive Care Unite with a high mortality. The underlying causes are uncontrolled inflammatory reactions and intractable hypoxemia, which are difficult to control and improve. In the past 10 years, gas medical studies have found that both hydrogen molecules and oxygen molecules have protective effects on acute lung injury by improving inflammatory reactions and hypoxia, respectively. Oxygen is an oxidant and hydrogen is an antioxidant. In this study, we investigated the combined effect of above two‐gas molecular on lipopolysaccharide (LPS) ‐induced acute lung injury. Methods To clarify whether the combination of hydrogen and oxygen could increase or cancel out the protective effect, an ALI mice model induced by intraperitoneal injection of LPS was established, and the degree of lung tissue and mitochondria damage was evaluated based on the pathological sections, inflammatory factors, wet–dry ratio, bronchoalveolar lavage fluid (BALF). Immunohistochemistry, electron microscopy, western blotting and other detection methods also used to evaluate the therapeutic effect on acute lung injury model. Results We observed that the combined protective effect of hydrogen and oxygen was superior to their respective protective effects, and the specific molecular mechanisms of the two therapies might be different. Conclusion Hydrogen plays a more important role in the inflammatory and anti‐apoptosis mechanisms, while oxygen improves hypoxia of the body, and thus, its molecular mechanism may be closely associated to the hypoxia pathways.
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