首页|氢气对内毒素小鼠急性肺损伤的影响

氢气对内毒素小鼠急性肺损伤的影响

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目的 探讨氢气对内毒素(LPS)诱导的急性肺损伤的影响及机制.方法 选择SPF级雄性ICR小鼠12只,6~8周龄,体质量25~35 g.采用随机数字表法将小鼠分为四组:对照组(C组)、吸入氢气组(H组)、肺损伤模型组(L组)和肺损伤模型+吸入氢气组(LH组),每组3只.C组不做处理;H组仅吸入4%氢气,持续12h;L组和LH组采用腹腔注射LPS 10 mg/kg建立肺损伤模型,LH组在建立肺损伤模型后即刻吸入4%氢气.于建模后12 h行肺超声检测肺水肿,超声检测完成后迅速处死小鼠,开胸取双肺组织,左肺组织采用Western blot法检测p-AMPK、p-ERK和p-p38蛋白含量,右肺组织采用HE染色行肺损伤评分并观察肺组织病理学改变.结果 与C组比较,L组和LH组B线面积明显增大,p-AMPK、p-ERK和p-p38蛋白含量明显升高(P<0.05);H组p-AMPK蛋白含量明显升高(P<0.05);L组肺损伤评分明显升高(P<0.05).与L组比较,LH组B线的面积明显减小,p-ERK、p-ERK和p-p38蛋白含量、肺损伤评分明显降低(P<0.05).C组和H组肺组织无红细胞渗漏,无水肿,无炎症细胞浸润,结构清晰可见.L组呈现出大量红细胞渗漏,炎性细胞浸润及肺间质水肿增厚.LH组肺部的出血、炎性细胞浸润和肺泡间隔增厚的情况减轻.结论 吸入4%氢气持续12 h可以通过上调p-AMPK、下调p-ERK/p-p38的表达,降低肺损伤评分,减轻LPS诱导的小鼠急性肺损伤.
Effect of hydrogen on lipopolysaccharide-induced acute lung injury in mice
Objective To investigate the mechanism of hydrogen alleviating lipopolysaccharide(LPS)-induced acute lung injury in mice.Methods The mice were randomly divided into four groups:control group(group C),hydrogen inhalation group(group H),lung injury model group(group L)and lung injury model+hydrogen inhalation group(group LH),3 mice in each group.Group C was not treated,and the acute lung injury model was established by intraperitoneal injection of LPS 10 mg/kg in groups L and LH.After the successful preparation of the lung injury model,the group LH received hydrogen interven-tion.Pulmonary edema was detected by pulmonary ultrasound 12 hours after modeling,then mice were sacri-ficed promptly.The left lung tissue was used to detect the protein of p-AMPK,p-ERK and p-p38.The right lung tissues were observed by HE staining for lung histopathological changes and lung injury score.Results Compared with group C,the B-line area in groups L and LH was significantly increased,and the protein contents of p-AMPK,p-ERK,and p-p38 were significantly increased(P<0.05),the protein contents of P-AMPK in group H was significantly increased(P<0.05),the lung injury score in group L was signifi-cantly increased(P<0.05).Compared with the group L,the B-line area,p-ERK,p-ERK and p-p38 pro-tein contents and lung injury score in group LH were significantly decreased(P<0.05).The lung tissue of groups C and H had no red blood cell leakage,no edema,no inflammatory cell infiltration,and the struc-ture was clearly visible.The group L showed a large number of red blood cell leakage,inflammatory cell in-filtration and pulmonary interstitial edema and thickening.Lung bleeding,inflammatory cell infiltration,and thickening of alveolar septa were reduced in the group LH.Conclusion Hydrogen alleviates endotoxin-in-duced lung injury in mice,possibly related to the upregulation of p-AMPK and downregulation of p-ERK/p-p38 expressions.

HydrogenLipopolysaccharideAcute lung injuryMitogen-activated protein kinases

施敏、李茜、昂扬、龙云、岳子川、罗冬雪、邵陆怡、周亚青、段满林、卞金俊、王晓琳

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200433 上海市,海军军医大学第一附属医院麻醉科

南京医科大学附属江宁医院麻醉科

南京大学医学院附属金陵医院麻醉科

南京大学医学院附属鼓楼医院疼痛医学科

南京市儿童医院麻醉科

昆山市第一人民医院麻醉科

江南大学附属医院疼痛科

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氢气 内毒素 急性肺损伤 丝裂原活化蛋白激酶

南京市医学科技发展项目

YKK21226

2024

临床麻醉学杂志
中华医学会南京分会

临床麻醉学杂志

CSTPCD北大核心
影响因子:2.225
ISSN:1004-5805
年,卷(期):2024.40(3)
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