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| 氢气对内毒素小鼠急性肺损伤的影响 |
| Effect of hydrogen on lipopolysaccharide-induced acute lung injury in mice |
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| DOI：10.12089/jca.2024.03.013 |
| 中文关键词: 氢气 内毒素 急性肺损伤 丝裂原活化蛋白激酶 |
| 英文关键词: Hydrogen Lipopolysaccharide Acute lung injury Mitogen-activated protein kinases |
| 基金项目:南京市医学科技发展项目（YKK21226） |
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| 中文摘要: |
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12 h；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。 |
| 英文摘要: |
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 intervention. Pulmonary edema was detected by pulmonary ultrasound 12 hours after modeling, then mice were sacrificed 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 significantly increased (P < 0.05). Compared with the group L, the B-line area, p-ERK, p-ERK and p-p38 protein 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 structure was clearly visible. The group L showed a large number of red blood cell leakage, inflammatory cell infiltration 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-induced lung injury in mice, possibly related to the upregulation of p-AMPK and downregulation of p-ERK/p-p38 expressions. |
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