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本文引用的文献

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Chemical constituents of tobacco smoke induce the production of interleukin-8 in human bronchial epithelium, 16HBE cells.烟草烟雾的化学成分可诱导人支气管上皮细胞16HBE细胞产生白细胞介素-8。
Tob Induc Dis. 2016 Jul 19;14:24. doi: 10.1186/s12971-016-0089-4. eCollection 2016.
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Relationship between knowledge about the harms of smoking and smoking status in the 2010 Global Adult Tobacco China Survey.2010年全球成人烟草调查中国部分中吸烟危害知识与吸烟状况之间的关系。
Tob Control. 2015 Jan;24(1):54-61. doi: 10.1136/tobaccocontrol-2013-051163. Epub 2013 Aug 29.
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A further review of inhalation studies with cigarette smoke and lung cancer in experimental animals, including transgenic mice.进一步回顾了实验动物(包括转基因小鼠)中香烟烟雾与肺癌的吸入研究。
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Roflumilast: first phosphodiesterase 4 inhibitor approved for treatment of COPD.罗氟司特:首个获批用于治疗慢性阻塞性肺疾病的磷酸二酯酶4抑制剂。
Drug Des Devel Ther. 2010 Jul 21;4:147-58. doi: 10.2147/dddt.s7667.
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PAH-DNA adducts, cigarette smoking, GST polymorphisms, and breast cancer risk.多环芳烃-DNA加合物、吸烟、谷胱甘肽S-转移酶基因多态性与乳腺癌风险
Environ Health Perspect. 2009 Apr;117(4):552-8. doi: 10.1289/ehp.0800119. Epub 2008 Dec 10.
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Platinum nanoparticle antioxidants inhibit pulmonary inflammation in mice exposed to cigarette smoke.铂纳米颗粒抗氧化剂可抑制暴露于香烟烟雾中的小鼠的肺部炎症。
Pulm Pharmacol Ther. 2009 Aug;22(4):340-9. doi: 10.1016/j.pupt.2008.12.015. Epub 2008 Dec 31.
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Future treatments for chronic obstructive pulmonary disease and its comorbidities.慢性阻塞性肺疾病及其合并症的未来治疗方法。
Proc Am Thorac Soc. 2008 Dec 1;5(8):857-64. doi: 10.1513/pats.200807-069TH.
8
Exposure level to cigarette tar or nicotine is associated with leukocyte DNA damage in male Japanese smokers.日本男性吸烟者接触香烟焦油或尼古丁的水平与白细胞DNA损伤有关。
Mutagenesis. 2008 Nov;23(6):451-5. doi: 10.1093/mutage/gen034. Epub 2008 Jun 27.
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An updated review of inhalation studies with cigarette smoke in laboratory animals.实验室动物吸入香烟烟雾研究的最新综述。
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10
Desensitization of PKA-stimulated ciliary beat frequency in an ethanol-fed rat model of cigarette smoke exposure.在乙醇喂养的香烟烟雾暴露大鼠模型中蛋白激酶A刺激的纤毛摆动频率脱敏
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[不同方式吸烟诱导大鼠急性肺损伤]

[Cigarette smoking in different manners induces acute lung injury in rats].

作者信息

Xiao Weiqiang, Zhou Guojun, Xu Chengyun, Xu Jian, Huang Fangfang, Lu Xinbo, Li Xia, Wu Ximei

机构信息

Technology Center, China Tobacco Zhejiang Industrial Co. Ltd, Hangzhou 310024, China.

Department of Pharmacology, Zhejiang University School of Medicine, Hangzhou 310058, China.

出版信息

Zhejiang Da Xue Xue Bao Yi Xue Ban. 2016 May 25;45(5):522-529. doi: 10.3785/j.issn.1008-9292.2016.09.11.

DOI:10.3785/j.issn.1008-9292.2016.09.11
PMID:28087913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10400824/
Abstract

To investigate the effects of cigarette smoking in different manners on acute lung injury in rats. The commercially available cigarettes with tar of 1,5, 11 mg were smoked in Canada depth smoking (health canada method, HCM) manner, and those with tar of 11 mg were also smoked in international standard (ISO) smoking manner. Rats were fixed and exposed to mainstream in a manner of nose-mouth exposure. After 28 days, the bronchoalveolar lavage fluids from left lung were collected for counting and classification of inflammatory cells and determination of pro-inflammatory cytokines IL-1β and TNF-α. The right lungs were subjected to histological examination and determination of myeloperoxidase (MPO) and superoxide dismutase (SOD) activities and glutathione, reactive oxygen species (ROS) and malondialdehyde (MDA) levels. In both HCM and ISO manners, the degree of lung injury was closely related to the tar content of cigarettes, and significant decrease in the body weight of rats was observed after smoking for one week. In a HCM manner, smoking with cigarette of 11 mg tar resulted in robust infiltration of macrophages, lymphocytes and neutrophils into lungs, significant increase in IL-1β and TNF-α levels and MPO activities, and significant decrease in GSH levels and SOD activities and increase in ROS and MDA levels (all <0.05). Smoking with cigarette of 5 mg tar led to moderate increase in IL-1β and TNF-α levels, and MPO activities (all <0.05), and moderate decrease in GSH levels and SOD activities and increase of ROS and MDA levels (all <0.05). However, smoking with cigarette of 1 mg tar affected neither inflammatory cell infiltration nor IL-1β and TNF-α levels. Cigarette smoking in nose-mouth exposure manner can induce acute lung injury in rats; and the degree of lung injury is closely related to the content of tar and other hazards in cigarettes.

摘要

探讨不同方式吸烟对大鼠急性肺损伤的影响。将焦油含量为1、5、11mg的市售香烟采用加拿大深度吸烟法(加拿大卫生部方法,HCM)吸烟,其中焦油含量为11mg的香烟也采用国际标准(ISO)吸烟法吸烟。将大鼠固定,采用口鼻暴露的方式使其接触主流烟雾。28天后,收集左肺支气管肺泡灌洗液,用于炎症细胞计数和分类以及促炎细胞因子IL-1β和TNF-α的测定。对右肺进行组织学检查,并测定髓过氧化物酶(MPO)和超氧化物歧化酶(SOD)活性以及谷胱甘肽、活性氧(ROS)和丙二醛(MDA)水平。在HCM和ISO两种吸烟方式下,肺损伤程度均与香烟焦油含量密切相关,且吸烟1周后大鼠体重显著下降。采用HCM吸烟方式时,吸焦油含量为11mg的香烟导致巨噬细胞、淋巴细胞和中性粒细胞大量浸润到肺中,IL-1β和TNF-α水平以及MPO活性显著升高,GSH水平和SOD活性显著降低,ROS和MDA水平升高(均P<0.05)。吸焦油含量为5mg的香烟导致IL-1β和TNF-α水平以及MPO活性中度升高(均P<0.05),GSH水平和SOD活性中度降低,ROS和MDA水平升高(均P<0.05)。然而,吸焦油含量为1mg的香烟对炎症细胞浸润以及IL-1β和TNF-α水平均无影响。口鼻暴露方式吸烟可诱导大鼠急性肺损伤;且肺损伤程度与香烟中焦油及其他有害物质的含量密切相关。