空气中PM2.5加重慢性阻塞性肺疾病模型小鼠肺损伤

doi:10.16352/j.issn.1001-6325.2026.01.0028

基础医学与临床 ›› 2026, Vol. 46 ›› Issue (1): 28-32.doi: 10.16352/j.issn.1001-6325.2026.01.0028

空气中PM2.5加重慢性阻塞性肺疾病模型小鼠肺损伤

倪兴^1*, 刘缝春², 鹿林¹, 毛韶华¹, 毕继蕊¹, 张润¹

1.安徽中医药大学第二附属医院呼吸科,安徽合肥 230000;
2.中国科学技术大学附属第一医院临床检验中心,安徽合肥 230000

收稿日期:2024-12-12 修回日期:2025-02-25 出版日期:2026-01-05 发布日期:2025-12-29
通讯作者: ^*1028870235@qq.com
基金资助:
安徽省高等学校科学研究重点项目(2023AH050750);安徽省重点研究与开发计划临床医学研究转化专项(202304295107020097);安徽中医药大学自然科学基金重点项目(2021efylc23)

PM2.5 in the air exacerbates lung injury in a mouse model of chronic obstructive pulmonary disease

NI Xing^1*, LIU Fengchun², LU Lin¹, MAO Shaohua¹, BI Jirui¹, ZHANG Run¹

1. Department of Respirology, the Second Affiliated Hospital of Anhui University of Chinese Medicine,Hefei 230000;
2. Center for Clinical Laboratory, the First Affiliated Hospital of University of Science and Technology of China,Hefei 230000,China

Received:2024-12-12 Revised:2025-02-25 Online:2026-01-05 Published:2025-12-29
Contact: ^*1028870235@qq.com

摘要/Abstract

摘要： 目的探究空气中细颗粒物(PM2.5)对慢性阻塞性肺疾病(COPD)模型小鼠肺损伤的加重作用,为后续研究提供可靠的实验依据。方法小鼠被随机分为对照组(control)、COPD组[烟熏和脂多糖(LPS)联合处理]、KP组[COPD模型小鼠鼻腔滴注肺炎克雷伯菌(KP)]、PM2.5组(COPD模型小鼠鼻腔滴注PM2.5)。采用肺功能检测用力肺活量(FVC)、深吸气量(IC)、第0.1秒用力肺活量(FEV_0.1)、第0.2秒用力肺活量(FEV_0.2)、0.1秒率(FEV_0.1/FVC)和0.2秒率(FEV_0.2/FVC);动脉血气分析氧分压(PaO₂)、二氧化碳分压(PaCO₂)、酸碱度(pH)和血氧饱和度(SaO₂);HE染色检测肺组织病理。结果与对照组相比,COPD组、KP组与PM2.5组小鼠FVC、IC、FEV_0.1、FEV_0.2和PaCO₂均显著升高(P＜0.05);FEV_0.1/FVC、FEV_0.2/FVC、PaO₂和SaO₂均显著下降(P＜0.05);肺组织病理显示典型的炎性反应和肺泡结构损伤。与COPD组相比,KP组与PM2.5组的FVC、FEV_0.1和FEV_0.2均显著增加(P＜0.05),FEV_0.1/FVC和FEV_0.2/FVC均显著降低,且PM2.5组的IC和PaCO₂升高(P＜0.05),SaO₂降低(P＜0.05);肺组织病理显示炎性反应和肺泡结构损伤进一步加重。结论 PM2.5能够进一步加剧COPD小鼠肺功能障碍,加重肺损伤。

关键词: 慢性阻塞性肺疾病, PM2.5, 肺功能, 肺损伤

Abstract: Objective To investigate the exacerbating effects of fine particulate matter (PM2.5) on lung injury in a chronic obstructive pulmonary disease (COPD) mouse model, and to provide a reliable experimental basis for further research. Methods Mice were randomly divided into four groups: control group, COPD group induced by cigarette smoke and lipopolysaccharide (LPS),KP group mice induced by intranasal instillation of Klebsiella pneumonia(KP),and PM2.5 group (COPD model) induced by intranasal instillation of PM2.5). Lung function test was used to check forced vital capacity (FVC), inspiratory capacity (IC), forced expiratory volume in 0.1 seconds (FEV0.1), FEV_0.2,FEV_0.1/FVC ratio and FEV_0.2/FVC ratio. Arterial blood gas analysis was applied to measure partial pressure of oxygen (PaO₂), partial pressure of carbon dioxide (PaCO₂), pH, and oxygen saturation (SaO₂). Lung histopathology was evaluated via hematoxylin-eosin (HE) staining microscopy. Results Compared with the control group,COPD,KP and PM2.5 groups showed significantly increased FVC,IC,FEV_0.1,FEV_0.2 and PaCO₂ (P＜0.05),along with significantly decreased FEV_0.1/FVC,FEV_0.2/FVC,PaO₂ and SaO₂ (P＜0.05). Histopathology microscopy showed typical inflammatory responses and alveolar structural damage. Compared with the COPD group,KP and PM2.5 groups exhibited further increases in FVC,FEV_0.1,and FEV_0.2(P＜0.05),reduced FEV_0.1/FVC and FEV_0.2/FVC ratios, elevated IC and PaCO₂ (PM2.5 group only,P＜0.05),and decreased SaO₂ (PM2.5 group only,P＜0.05). Histopathology microscopy confirmed aggravated inflammatory responses and alveolar destruction in these groups. Conclusions PM2.5 exacerbates pulmonary dysfunction and lung injury in COPD mice.

Key words: chronic obstructive pulmonary disease, PM2.5, pulmonary function, lung injury

中图分类号:

R332

倪兴, 刘缝春, 鹿林, 毛韶华, 毕继蕊, 张润. 空气中PM2.5加重慢性阻塞性肺疾病模型小鼠肺损伤[J]. 基础医学与临床, 2026, 46(1): 28-32.

NI Xing, LIU Fengchun, LU Lin, MAO Shaohua, BI Jirui, ZHANG Run. PM2.5 in the air exacerbates lung injury in a mouse model of chronic obstructive pulmonary disease[J]. Basic & Clinical Medicine, 2026, 46(1): 28-32.

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空气中PM2.5加重慢性阻塞性肺疾病模型小鼠肺损伤

PM2.5 in the air exacerbates lung injury in a mouse model of chronic obstructive pulmonary disease

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