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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OA

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

中文摘要英文摘要

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(FEV0.1)、第 0.2 秒用力肺活量(FEV0.2)、0.1 秒率(FEV0.1/FVC)和 0.2 秒率(FEV0.2/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、FEV0.1、FEV0.2和PaCO2 均显著升高(P<0.05);FEV0.1/FVC、FEV0.2/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、FEV0.1和FEV0.2均显著增加(P<0.05),FEV0.1/FVC和 FEV0.2/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.

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 pneu-monia(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),FEV0.2,FEV0.1/FVC ratio and FEV0.2/FVC ratio.Arterial blood gas analysis was applied to measure partial pressure of oxygen(PaO2),partial pressure of carbon dioxide(PaCO2),pH,and oxygen satura-tion(SaO2).Lung histopathology was evaluated via hematoxylin-eosin(HE)staining microscopy.Results Com-pared with the control group,COPD,KP and PM2.5 groups showed significantly increased FVC,IC,FEV0.1,FEV0.2 and PaCO2(P<0.05),along with significantly decreasedFEV0.1/FVC,FEV0.2/FVC,PaO2 and SaO2(P<0.05).Histo-pathology microscopy showed typical inflammatory responses and alveolar structural damage.Compared with the COPD group,KP and PM2.5 groups exhibited further increases in FVC,FEV0.1,and FEV0.2(P<0.05),reducedFEV0.1/FVC and FEV0.2/FVC ratios,elevated IC and PaCO2(PM2.5 group only,P<0.05),and decreased SaO2(PM2.5 group on-ly,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.

倪兴;刘缝春;鹿林;毛韶华;毕继蕊;张润

安徽中医药大学第二附属医院 呼吸科,安徽 合肥 230000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安徽中医药大学第二附属医院 呼吸科,安徽 合肥 230000安徽中医药大学第二附属医院 呼吸科,安徽 合肥 230000安徽中医药大学第二附属医院 呼吸科,安徽 合肥 230000安徽中医药大学第二附属医院 呼吸科,安徽 合肥 230000

医药卫生

慢性阻塞性肺疾病PM2.5肺功能肺损伤

chronic obstructive pulmonary diseasePM2.5pulmonary functionlung injury

《基础医学与临床》 2026 (1)

28-32,5

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)

10.16352/j.issn.1001-6325.2026.01.0028

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