不同吸烟量对大鼠气道上皮细胞中细胞间黏附分子1表达的影响  

Effects of different smoking quantity on expressions of intercellular adhesion molecule-1 in rat airway endothelial cells

作　　者：索耀君[1] 许建英[1] 

机构地区：[1]山西医科大学第一医院呼吸科,太原030001

出　　处：《国际呼吸杂志》2009年第9期534-537,共4页International Journal of Respiration

摘　　要：目的通过研究不同吸烟量、不同吸烟持续时间吸烟及戒烟对大鼠气道上皮细胞中细胞间黏附分子1（intercellular adhesion molecule-1，ICAM-1）mRNA及其蛋白水平表达的影响，探讨吸烟和戒烟与慢性阻塞性肺疾病气道炎症的关系。方法雄性Wistar大鼠40只，随机分为对照组、长期大量吸烟组、长期小量吸烟组、短期大量吸烟组、长期大量吸烟后戒烟组，每组各8只，用原位杂交法及免疫组织化学法检测ICAM-1mRNA及其蛋白在各组大鼠气道上皮细胞中的表达。结果与对照组ICAM-1 mRNA及其蛋白（1．45±0．98，8．83±0．77）水平比较，长期大量吸烟组（6．93±1．44，19．22±0．22）、短期大量吸烟组（2．92±0．67，12．91±1．31）、长期小量吸烟组（4．76±0．68，14．03±2．39）、长期大量吸烟后戒烟组（4．84±0．94，14．95．±1．82）表达均明显升高，以长期大量吸烟组最为显著，差异均具有统计学意义（P〈0．05）。与长期大量吸烟组相比，长期小量吸烟组、短期大量吸烟组、长期大量吸烟后戒烟组ICAM-1 mRNA及其蛋白水平均低于长期大量吸烟组，差异均具有统计学意义（P〈0．05）。结论吸烟引起大鼠气道上皮细胞ICAM-1 mRNA及其蛋白的表达水平升高，并随吸烟时间和量的增加其表达增加，戒烟后其表达可下降。提示戒烟可减轻气道炎症，是预防慢性阻塞性肺疾病的有效措施。Objective To study the relationship between smoking as well as smoke abatement and airway inflammation of chronic obstructive pulmonary disease （COPD） through researching effects of different smoking quantity and different smoking time, smoking and smoke abatement on expression of intercellular adhesion molecule-1 （ICAM-1） in airway endothelial cells in rat model of smoking. Methods Forty Wistar rats were randomly divided into control group, long-term multiplicity smoking group, long-term manipulus smoking group, short-term multiplicity smoking group and smoke abatement group, eight rats in a group. The expressions of ICAM-1 in airway endothelial cells of rats were detected by immunohistochemistry and hybridization in situ. Results The expression of ICAM-1 mRNA and protein level in bronchial endothelial cells of long-term multiplicity smoking group were （ 6.93 ± 1.44, 19.22 ± 0.22）, short-term multiplicity smoking group （ 2.92 ± 0.67,12.91 ± 1.31 ）, long-term manipulus smoking group （4.76 ± 0.68, 14.03 ± 2.39） and smoke abatement group （4.84 ± 0.94,14.95 ± 1.82）, which were significantly increased compared with those of control group （ 1.45 ± 0.98,8.83 ± 0.77）, peaking in the long-term muhiplieity smoking group（ P 〈0.05）. The expression of ICAM-1 in bronchial endothelial cells of long-term manipulus smoking group,short-term multiplicity smoking group, smoke abatement group and the control group were lower than that of long-term multiplicity smoking group（ P 〈0.05）. Conclusions Smoking can result in the high expression of ICAM-1 mRNA and protein level in airway endothelial cells of rat model. The expression of ICAM-1 mRNA and protein level increase with the augmentation of smoking time and quantity and decrease after smoke abatement. It means smoke abatement can relieve airway inflammation but can not eliminate the change. Smoking abatement is an effective measure of preventing COPD.

关 键 词：吸烟 慢性阻塞性肺疾病 细胞间黏附分子1 

分 类 号：R5[医药卫生—内科学]