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| 香烟烟雾中5-羟甲基-2-糠醛诱发小鼠肺气肿的作用研究 |
| 作者：段名秀 王丽 彭梦凡 夏蓉 王守林 |
| 单位：南京医科大学公共卫生学院 现代毒理学教育部重点实验室, 江苏 南京 211166 |
| 关键词：香烟烟雾 5-羟甲基-2-糠醛 尼古丁 肺气肿 粒细胞-巨噬细胞集落刺激因子 小鼠 |
| 分类号：R-33; R163.2 |
| 出版年·卷·期（页码）：2025·44·第四期（534-540） |
| 摘要： |
| 目的:评价香烟烟雾中重要组分5-羟甲基-2-糠醛(5-HMF)对小鼠肺气肿形成的影响。方法:前期将香烟烟雾抽提物(CSE)经液液萃取联合葡聚糖凝胶LH-20分离出5-HMF(CSE-HMF)、尼古丁(CSE-Nicotine)以及剩余组分(CSE-rCAP)。采用气管滴注方法构建小鼠染毒模型,采用肺通气功能、肺泡平均线性截距(MLI)、肺组织炎症细胞及炎症因子等指标,综合评估CSE-HMF及其它CSE组分对小鼠肺气肿形成的影响。结果:CSE中5-HMF和尼古丁组分染毒小鼠均出现了较为明显的肺通气功能下降、MLI增大和炎症细胞浸润等肺气肿表型,其中气道狭窄指数(Penh)分别上升了13%、20%,MLI均升高了50%左右,炎症细胞浸润程度评分均为对照组的3.7倍左右;两组染毒小鼠的血液和支气管肺泡灌洗液(BALF)中与肺气肿形成相关的嗜酸粒细胞比率(EOS%)也显著增高(P<0.05),但仅CSE-HMF组小鼠BALF中的粒细胞-巨噬细胞集落刺激因子(GM-CSF)较对照组明显升高(P<0.01)。结论:5-HMF可能是CSE中促进肺气肿形成的新的重要毒性组分,GM-CSF可能是潜在的效应指标。 |
| Objective: To evaluate the effects of 5-hydroxymethyl-2-furfural(5-HMF), an important component of cigarette smoke, on the formation of emphysema in mice. Methods: In the early stage, cigarette smoke extract(CSE) was separated by liquid-liquid extraction combined with glucan gel LH-20 to obtain 5-HMF(CSE-HMF), nicotine(CSE-Nicotine), and the remaining components(CSE-rCAP). The mouse exposure model was constructed by tracheal instillation. Indicators such as lung ventilation function, mean linear distance of alveoli(MLI), inflammatory cells and inflammatory factors in lung tissue were used to comprehensively evaluate the effects of CSE-HMF and other CSE components on the formation of emphysema in mice. Results: The mice exposed to 5-HMF and nicotine in CSE showed obvious emphysema phenotypes such as decreased pulmonary ventilation function, increased MLI and inflammatory cell infiltration, in particular, the enhanced pause(Penh) index increased by 13% and 20% respectively, MLI increased by approximately 50% in both groups, and the inflammatory cell infiltration scores were about 3.7 times higher than those in the control group. The eosinophil ratio(EOS%) related to emphysema formation in blood and bronchoalveolar lavage fluid(BALF) in the two groups also increased significantly(P<0.05), but only the granulocyte-macrophage colony-stimulating factor(GM-CSF) in the BALF of the CSE-HMF group was significantly higher than that of the control group(P<0.01). Conclusion: 5-HMF might be a novel important toxic component in CSE to promote the formation of emphysema, and GM-CSF might be a potential effect index. |
| 参考文献： |
| [1] WHO global report on trends in prevalence of tobacco use 2000—2030[EB/OL].[2025-03-26].https://www.who.int/publications/i/item/9789240088283. [2] TANABE N,MURO S,HIRAI T,et al.Impact of exacerbations on emphysema progression in chronic obstructive pulmonary disease[J].Am J Respir Crit Care Med,2011,183(12):1653-1659. [3] WU H,MA H,WANG L,et al.Regulation of lung epithelial cell senescence in smoking-induced COPD/emphysema by microR-125a-5p via Sp1 mediation of SIRT1/HIF-1a[J].Int J Biol Sci,2022,18(2):661-674. [4] ZENG T,LIU Y,JIANG Y,et al.Advanced materials design for adsorption of toxic substances in cigarette smoke[J].Adv Sci(Weinh),2023,10(22):e2301834. [5] OZGA J E,SARGENT J D,STEINBERG A W,et al.Childhood cigarette smoking and risk of COPD in older United States adults:a nationally representative replication study[J].Chronic Obstr Pulm Dis,2024,11(6):549-557. [6] THOMSON N C,POLOSA R,SIN D D.Cigarette smoking and asthma[J].J Allergy Clin Immunol Pract,2022,10(11):2783-2797. [7] 程迪,吕镗烽.肺癌患者免疫检查点抑制剂相关肺炎的危险因素及临床特点[J].东南大学学报(医学版),2024,43(4):516-522. [8] 刘静,刘洪梅,夏长金,等.唐山地区老年肺癌高危人群早期筛查结果及危险因素分析[J].现代医学,2022,50(3):320-324. [9] JI M,ZHANG Z,LI N,et al.Identification of 5-hydroxymethylfurfural in cigarette smoke extract as a new substrate metabolically activated by human cytochrome P450 2A13[J].Toxicol Appl Pharmacol,2018,359:108-117. [10] CHEN X,TU Q,ZHAO W,et al.5-hydroxymethylfurfural mediated developmental toxicity in Drosophila melanogaster[J].Food Chem Toxicol,2024,189:114738. [11] ZHUANG T,GAO C,ZENG W,et al.Analysis of key targets for 5-hydroxymethyl-2-furfural-induced lung cancer based on network toxicology,network informatics,and in vitro experiments[J].Drug Chem Toxicol,2025,48(2):451-461. [12] 王明磊,王文革,张俊红.黄芪甲苷对哮喘模型小鼠气道炎症及IL-22的影响[J].军事医学,2017,41(7):581-585. [13] GODBOLE S,BOWLER R P.Metabolome features of COPD:a scoping review[J].Metabolites,2022,12(7):621. [14] LIN J,XIA H,YU J,et al.circADAMTS6 via stabilizing CAMK2A is involved in smoking-induced emphysema through driving M2 macrophage polarization[J].Environ Int,2024,190:108832. [15] TIAN X,WANG S,ZHANG C,et al.Blocking IL-23 signaling mitigates cigarette smoke-induced murine emphysema[J].Environ Toxicol,2024,39(12):5334-5346. [16] CHERIAN S V,KUMAR A,ESTRADA-Y-MARTIN R M.E-cigarette or vaping product-associated lung injury:a review[J].Am J Med,2020,133(6):657-663. [17] BANZATO R,PINHEIRO N M,OLIVO C R,et al.Long-term endogenous acetylcholine deficiency potentiates pulmonary inflammation in a murine model of elastase-induced emphysema[J].Sci Rep,2021,11(1):15918. [18] XU X,YU T,DONG L,et al.Eosinophils promote pulmonary matrix destruction and emphysema via cathepsin L[J].Signal Transduct Target Ther,2023,8(1):390. [19] TANABE N,HOSHINO Y,MARUMO S,et al.Thioredoxin-1 protects against neutrophilic inflammation and emphysema progression in a mouse model of chronic obstructive pulmonary disease exacerbation[J].PLoS One,2013,8(11):e79016. |
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