Progress in researches on effect of PM2.5 on occurrence and development of chronic obstructive pulmonary disease and medication of the disease
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摘要: 慢性阻塞性肺疾病(慢阻肺)是一种以气流受限为特征可以预防和治疗的疾病,与肺部对有害气体的异常炎症及免疫反应有关。目前环境问题受到广泛关注,细颗粒物(PM2.5)作为危害严重的环境污染物,其对健康的影响不容忽视。研究表明PM2.5在慢阻肺发生发展的过程中起到重要作用。PM2.5主要通过氧化应激、炎症反应和免疫功能失衡影响慢阻肺的进展。本文从慢阻肺危险因素入手,综述PM2.5对慢阻肺疾病发生发展影响的可能机制,分析不同药物对PM2.5影响下慢阻肺进展的干预, 为慢阻肺的预防与治疗提供新的思路。
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关键词:
- 细颗粒物(PM2.5) /
- 慢性阻塞性肺疾病(慢阻肺) /
- 药物治疗
Abstract: Chronic obstructive pulmonary disease, characterized by chronic airflow limitation and being preventable and curable, is usually associated with some abnormal inflammatory response induced by hazardous gases. Recent studies have demonstrated that particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) may exert a regulatory effect on chronic obstructive pulmonary disease. The study summarized the occurrence and development of the chronic obstructive pulmonary disease and analyzed the progress in medication of the disease for the prevention and control of the disease. -
[1] Rycroft CE, Heyes A, Lanza L, et al. Epidemiology of chronic obstructive pulmonary disease: a literature review[J]. Int J Chron Obstruct Pulmon Dis, 2012, 7: 457 – 494. [2] Zhong N, Wang C, Yao W, et al. Prevalence of chronic obstructive pulmonary disease in China: a large population-based survey[J]. Am J Rspire Crit Care Med, 2007, 176(8): 753 – 760. doi: 10.1164/rccm.200612-1749OC [3] 中华医学会呼吸分会慢性阻塞性肺疾病组. 慢性阻塞性肺疾病诊治指南[J]. 中华实用结核和呼吸杂志, 2008, 25(8): 453 – 460. [4] Cortez-Luqo M, Ramirez-Aquilar M, Pere-Padilla R, et al. Effect of personal exposure to PM2.5 on respiratory health in a Mexican Panel of patients with COPD[J]. Int J Environ Res Public Health, 2015, 12(9): 10635 – 10647. doi: 10.3390/ijerph120910635 [5] Tsai SS, Yang CY. Fine particulate air pollution and hospital admissions for pneumonia in a subtropical city: Taipei, Taiwan[J]. J Toxicol Environ Health A, 2014, 77(4): 192 – 201. doi: 10.1080/15287394.2013.853337 [6] Qin X, Li X, Wang S, et al. Fine particulate air pollution and hospital emergency room visits for respiratory disease in urban areas in Beijing, China, in 2013[J]. PLoS One, 2016, 11(4): e0153099. doi: 10.1371/journal.pone.0153099 [7] Zhou Z, Liu Y, Duan F, et al. Transcriptomic analyses of the biological effects of airborne PM2.5 exposure on human bronchial epithelial cells[J]. PLoS One, 2015, 10(9): e0138267. doi: 10.1371/journal.pone.0138267 [8] Boveris A, Chance B. The mitochondrial generatation of hydrogen peroxide. General properties and effect of hyperbaric oxygen[J]. Biochemical Journal, 1973, 143(3): 707 – 716. [9] Kirkham PA, Barnes PJ. Oxidative stress in COPD[J]. Chest, 2013, 144(1): 266 – 273. doi: 10.1378/chest.12-2664 [10] Stockley RA. Neutrophils and the pathogenesis of COPD[J]. Chest, 2002, 121: 151S – 155S. doi: 10.1378/chest.121.5_suppl.151S [11] Kirkham PA, Caramori G, Casolari P, et al. Oxidative stress-induced antibodies to carbonyl-modified protein correlate with severity of chronic obstructive pulmonary disease[J]. Am J Respir Crit Care Med, 2011, 184(7): 796 – 802. doi: 10.1164/rccm.201010-1605OC [12] Kirkham PA, Spooner G, Rahman I, et al. Macrophage phagocytosis of apoptotic neutrophils is compromised by matrix protein modified by cigarette smoke and lipid peroxidation products[J]. Biochem Biophys Res Commun, 2004, 318(1): 32 – 37. doi: 10.1016/j.bbrc.2004.04.003 [13] Henricks PA, Nijkamp FP. Reactive oxygen species as mediators in asthma[J]. Pulm Pharmacol Ther, 2001, 14(6): 409 – 420. doi: 10.1006/pupt.2001.0319 [14] Lee W, Thomas PS. Oxidative stress in COPD and its measurement through exhaled breath condensate[J]. Clin Transl Sci, 2009, 2(2): 150 – 155. doi: 10.1111/cts.2009.2.issue-2 [15] Macnee W. Pulmonary and systemic oxidant/antioxidant imbalance in chronic obstructive pulmonary disease[J]. Proceedings of the American Thoracic Society, 2005, 2(1): 50 – 60. doi: 10.1513/pats.200411-056SF [16] Ito K, Barnes PJ. COPD as a disease of accelerated lung aging[J]. Chest, 2009, 135(1): 173 – 180. doi: 10.1378/chest.08-1419 [17] Rosanna DP, Salvatore C. Reactive oxygen species, inflammation, and lung diseases[J]. Curr Pharm Des, 2012, 18(26): 3889 – 3990. doi: 10.2174/138161212802083716 [18] Kirkham PA, Spooner G, Ffoulkes-Jones C, et al. Cigarette smoke triggers macrophage adhesion and activation role of lipid peroxidation products and scavenger receptor[J]. Free Radic Biol Med, 2003, 35(7): 697 – 710. doi: 10.1016/S0891-5849(03)00390-3 [19] 邓晓蓓, 张芳, 丁文军. PM-(2.5)诱导的氧化应激在肺上皮细胞自噬和凋亡的分子作用机制[C]. 乌鲁木齐: 第一届国际暨第十三次中国生物物理学术大会, 2013: 1. [20] 李东繁, 杜旭升, 刘安. PM-(2.5)对大鼠气管上皮细胞氧化应激及自噬的影响[J]. 陕西医学杂志, 2017(01): 3 – 4, 12. doi: 10.3969/j.issn.1000-7377.2017.01.001 [21] 赵启君, 刘晓菊, 曾晓丽, 等. 细颗粒物对慢性阻塞性肺疾病小鼠肺组织Nrf2水平的影响及其与氧化应激的关系[J]. 中华医学杂志, 2016, 28(96): 2241 – 2245. [22] Grevendonk L, Jansse BG, Vanpoucke C, et al. Mitochondrial oxidative DNA damage and exposure to particulate air pollution in mother-newborn pairs[J]. Environ Health, 2016, 15(1): 10. doi: 10.1186/s12940-016-0095-2 [23] Wang G, Zhao J, Jiang R, et al. Rat lung response to ozone and fine particulate matter (PM2.5) exposures[J]. Environ Toxicol, 2015, 30(3): 343 – 356. doi: 10.1002/tox.v30.3 [24] Angelis N, Porpodis K, Zarogoulidis P, et al. Airway inflammation in chronic obstructive pulmonary disease[J]. J Thorac Dis, 2014, 6(Suppl 1): S167 – 172. [25] Ling SH, van Eeden SF. Particulate matter air pollution exposure: role in the development and exacerbation of chronic obstructive pulmonary disease[J]. Int J Chron Obstruct Pulmon Dis, 2009, 4(1): 233 – 243. [26] Zhao Q, Chen H, Yang T, et al. Direct effects of airborne PM2.5 exposure on macrophage polarizations[J]. Biochim Biophys Acta, 2016, 1860(12): 2835 – 2843. doi: 10.1016/j.bbagen.2016.03.033 [27] 徐秀段, 敖登其格木, 刘莎莎, 等. PM2.5通过诱导AP-1活化介导支气管上皮细胞中VEGF的诱导表达和炎症反应[J]. 军事医学, 2016(07): 541 – 544. [28] 姜智海, 宋伟民, 周晓瑜, 等. PM-(2.5)对小鼠肺急性损伤的试验研究[J]. 卫生研究, 2004(3): 264 – 266. doi: 10.3969/j.issn.1000-8020.2004.03.003 [29] Wang H, Song L, Ju W, et al. The acute airway inflammation induced by PM2.5 exposure and the treatment of essential oils in Balb/c mice[J]. Sci Rep, Sci Rep, 2017, 7: 44256. doi: 10.1038/srep44256 [30] Song L, Li D, Li X, et al. Exposure to PM2.5 induces abrrant activation of NF-kappa B in human airway epithelial cells by downregulating miR-331 expression[J]. Environ Toxicol Pharmacol, 2017, 50: 192 – 199. doi: 10.1016/j.etap.2017.02.011 [31] 钱文君, 王佩芳, 徐慧, 等. 慢性阻塞性肺疾病病人外周血T淋巴细胞的检测及意义[J]. 中国老年学杂志, 2014(16): 4501 – 4502. doi: 10.3969/j.issn.1005-9202.2014.16.041 [32] 陈昌枝, 邵有和, 覃家盟, 等. 慢性阻塞性肺疾病患者免疫球蛋白的表达及与肺功能的关系[J]. 临床肺科杂志, 2015, 20(8): 1404 – 1408. doi: 10.3969/j.issn.1009-6663.2015.08.015 [33] Urboniene D, Babusyte A, Lӧtvall J, et al. Distribution of γδ and other T-lymphocyte subsets in patients with chronic obstructive pulmonary disease and asthma[J]. Respire Med, 2013, 107(3): 413 – 425. doi: 10.1016/j.rmed.2012.11.012 [34] Migliaccio CT, Kobos E, King QO, et al. Adverse effects of wood smoke PM(2.5) exposure on macrophage functions[J]. Inhal Toxicol, 2013, 25(2): 67 – 76. doi: 10.3109/08958378.2012.756086 [35] Zelikoff JT, Chen LC, Cohen MD, et al. Effects of inhaled ambient particulate matter on pulmonary antimicrobial immune defense[J]. Inhal Toxicol, 2003, 15(2): 131 – 150. doi: 10.1080/08958370304478 [36] 褚旭. PM2.5加剧慢性阻塞性肺疾病小鼠肺泡巨噬细胞吞噬功能障碍及对免疫炎症反应的影响[D]. 兰州: 兰州大学博士学位论文, 2017. [37] 邱敬满. 黄芪水提物及黄芪多糖对PM2.5致慢性阻塞性疾病小鼠肺泡巨噬细胞吞噬能力下降的保护作用[D]. 兰州: 兰州大学硕士学位论文, 2015. [38] Sun WY, Wei W, Gui SY, et al. Protective effect of extract from Paeonia lactiflora and Astragalus membranaceus against liver injury induced by bacillus Calmette-Guerin and lipopolysaccharide in mice[J]. Basic Clin Pharmacol Toxicol, 2008, 103: 143 – 149. doi: 10.1111/pto.2008.103.issue-2 [39] Liu Y, Liu F, Yang Y, et al. Astragalus polysaccharide ameliorates ionizing radiation-induced oxidative stress in mice[J]. Int J Biol Macromol, 2014, 68: 209 – 214. doi: 10.1016/j.ijbiomac.2014.05.001 [40] 谷明杰. 固本止咳中药对PM2.5致小鼠肺损伤模型肺组织TNF-α、IL-8、SIgA的影响[D]. 北京: 北京中医药大学硕士学位论文, 2016.
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