| LPS诱导急性肺损伤中中性粒细胞的病理作用及干预研究 |
| 投稿时间：2025-07-30 修订日期：2025-08-13 点此下载全文 |
| 引用本文：陈佳慧,高晞,温笑,梅熠闻,邵礼飞,孙炳伟.LPS诱导急性肺损伤中中性粒细胞的病理作用及干预研究[J].医学研究杂志,2026,55(1):42-48 |
| DOI：
10.11969/j.issn.1673-548X.2026.01.009 |
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| 作者 | 单位 | | 陈佳慧 | 南京医科大学附属苏州医院烧伤整形科 苏州,215002 通信作者:孙炳伟,电子信箱:sunbinwe@hotmail.com〖JZ | | 高晞 | 南京医科大学附属苏州医院烧伤整形科 苏州,215002 通信作者:孙炳伟,电子信箱:sunbinwe@hotmail.com〖JZ | | 温笑 | 南京医科大学附属苏州医院烧伤整形科 苏州,215002 通信作者:孙炳伟,电子信箱:sunbinwe@hotmail.com〖JZ | | 梅熠闻 | 南京医科大学附属苏州医院烧伤整形科 苏州,215002 通信作者:孙炳伟,电子信箱:sunbinwe@hotmail.com〖JZ | | 邵礼飞 | 南京医科大学附属苏州医院烧伤整形科 苏州,215002 通信作者:孙炳伟,电子信箱:sunbinwe@hotmail.com〖JZ | | 孙炳伟 | 南京医科大学附属苏州医院烧伤整形科 苏州,215002 通信作者:孙炳伟,电子信箱:sunbinwe@hotmail.com〖JZ |
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| 基金项目:国家自然科学基金资助项目(U21A20370)；国家自然科学基金资助项目(面上项目)(82072217) |
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| 中文摘要:目的 探讨LPS诱导的急性肺损伤时,中性粒细胞介导肺损伤的病理作用及干预研究。方法 将24只7周龄雄性C57BL/6J小鼠随机分为4组,即对照组、脂多糖(lipopolysaccharide,LPS)模型组、西维来司他钠(Sivelestat Sodium)干预组(SV+LPS组)、地塞米松(dexamethasone)干预组(DEX+LPS组),每组6只。通过气道内雾化LPS(10mg/kg)诱导急性肺损伤模型。通过HE染色和肺组织湿/干比(W/D)评估肺组织病理损伤及水肿程度；流式微球阵列技术(cytometric bead array,CBA)检测支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中炎性细胞因子水平；免疫荧光和免疫组织化学染色法分别检测中性粒细胞浸润及中性粒细胞弹性蛋白酶(neutrophil elastase,NE)含量。结果 与对照组比较,LPS模型组肺泡腔内渗出、肺间质增厚及肺水肿程度显著加重(P＜0.05),肺内中性粒细胞浸润,NE含量及BALF中炎性细胞因子含量显著升高(P＜0.05)；与LPS模型组比较,SV+LPS组和DEX+LPS组肺泡渗出、间质增厚、肺水肿及BALF炎性细胞因子水平均显著减轻(P<0.05),但两组中性粒细胞浸润数无显著减少(P>0.05)；其中DEX+LPS组肺组织NE含量显著降低(P<0.05),而SV+LPS组NE水平无显著变化。结论 LPS诱导的急性肺损伤时中性粒细胞肺内浸润并释放NE导致肺损伤,SV作为NE竞争性抑制剂,DEX作为膜稳定剂抑制中性粒细胞活化,均减轻LPS诱导的小鼠肺水肿及肺部炎症。 |
| 中文关键词:急性肺损伤 中性粒细胞弹性蛋白酶 西维来司他钠 地塞米松 |
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| Pathological Role and Intervention Study of Neutrophils in LPS-induced Acute Lung Injury. |
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| Abstract:Objective To explore the mechanism of neutrophil-mediated lung injury and the efficacy of interventions in lipopolysaccharide (LPS)-induced acute lung injury. Methods Twenty-four 7-week-old male C57BL/6J mice were randomly assigned to four groups:control group, LPS model group, Sivelestat Sodium (SV) intervention group (SV+LPS group), and dexamethasone (DEX) intervention group (DEX+LPS group), with six mice in each group. ALI was induced by intranasal nebulization of LPS (10mg/kg). Lung pathological damage and edema were evaluated via hematoxylin-eosin (HE) staining and lung wet/dry weight ratio (W/D). Inflammatory factors in bronchoalveolar lavage fluid (BALF) were measured using cytometric bead array (CBA). The levels of neutrophil infiltration and neutrophil elastase (NE) were detected by immunofluorescence and immunohistochemistry, respectively. Results Compared with the control group, the LPS model group showed significantly increased alveolar exudation, interstitial thickening, and pulmonary edema (P<0.05), along with elevated neutrophil infiltration, NE content in lung tissue, and inflammatory factor levels in BALF (P<0.05). Compared with the LPS model group, both SV+LPS group and DEX+LPS group exhibited reduced alveolar exudation, interstitial thickening, pulmonary edema, and BALF inflammatory factors (P<0.05), but no significant decrease in neutrophil infiltration (P>0.05). Notably, DEX significantly reduced NE levels in lung tissue (P<0.05), while SV had no such effect. Conclusion LPS induces lung injury via neutrophil infiltration and NE release in acute lung injury. SV as a competitive inhibitor of NE, and DEX as a membrane stabilizer that inhibits neutrophil activation, both alleviate LPS-induced pulmonary edema and inflammation in mice. |
| keywords:Acute lung injury Neutrophil elastase Sevelamer Dexamethasone |
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