| Objective:To study the relationship between smoking as well as smoke abatement and airway inflammation of chronic obstructive pulmonary disease(COPD) though 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 the control group,long-term multiplicity smoking group,long-term manipulus smoking group,short-term multiplicity smoking group and smoke abatement group,there are eight in every group.Rat smoking device was in accordance with Xusanlin smoking device.Establish long-term multiplicity smoking group through breathing in cigarette smoke for 20 weeks,breathing cigarette twice a day and breathing ten cigarettes every time,breathing cigarette for six days in a week.Establish long-term manipulus smoking group through breathing in cigarette smoke for 20 weeks, breathing cigarette twice a day and breathing five cigarettes every time,breathing cigarette for six days in a week.Establish short-term multiplicity smoking group through breathing in cigarette smoke for 10 weeks,breathing cigarette twice a day and breathing ten cigarettes every time,breathing cigarette for six days in a week.Establish smoke abatement group through breathing in cigarette smoke for 20 weeks and breaking away from smoke for 10 weeks.Observe the histopathology change and detect the expressions of ICAM-1mRNA and its protein in airway endothelial cells of rats using immunohistochemistry and hybridization in situ respectively.Results:1 Histopathology change:The alveolar structure of the control group is normal and continuous,small bronchial glands have no inflammatory cell infiltration,alveolar wall is integral,and long-term multiplicity smoking group,long-term manipulus smoking group,short-term multiplicity smoking group,and smoke abatement group exist in varying degrees of alveolar wall thinning or rupture,such as alveolar structure disorder,respiratory bronchiole of the existence of cystic dilatation,alveolar structure integration into the wall and infiltration of a large number of mononuclear cells and lymphocyte,Ciliated epithelial broken off,reduction of the number of cilia,peaking in the long-term multiplicity smoking group.2 The expression of ICAM-1 protein level in bronchial endothelial cells The expression of ICAM-1 protein level in bronchial endothelial cells of long-term multiplicity smoking group (19.22±0.22),short-term multiplicity smoking group(12.91±1.31),long-term manipulus smoking group(14.03±2.39) and smoke abatement group(14.95±1.82),significantly increased compared to that of the control group(8.83±0.77),peaking in the long-term multiplicity smoking group(P<0.05).Compared to the expression of ICAM-1 protein level in bronchial endothelial cells of long-term multiplicity smoking group,that of short-term multiplicity smoking group,long-term manipulus smoking group,smoke abatement group and the control group decreased. (P<0.05)3 The expression of ICAM-1 mRNA level in bronchial endothelial cells The expression of ICAM-1 mRNA level in bronchial endothelial cells of long-term multiplicity smoking group (6.93±1.44),short-term multiplicity smoking group(2.92±0.67),long-term manipulus smoking group(4.76±0.68) and smoke abatement group(4.84±0.94),was significantly increased compared to that of the control group(1.45±0.98),peaking in the long-term multiplicity smoking group(P<0.05).Compared to the expression of ICAM-1 mRNA level in bronchial endothelial cells of long-term multiplicity smoking group,that of short-term multiplicity smoking group,long-term manipulus smoking group,smoke abatement group and the control group decreased (P<0.05).The expression of ICAM-1 mRNA level in bronchial endothelial cells of long-term manipulus smoking group was higher than that of short-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 increases with the augmentation of smoking time and quantity and decreases after smoke abatement.It means smoke abatement can relieve airway inflammation but cannot eliminate the change.Smoking abatement is a effective measure of preventing COPD. |