烟草烟雾暴露对支气管哮喘小鼠肺组织CB2受体mRNA及其蛋白表达的影响

Effect of tobacco smoke exposure on the expression of CB2 receptor＇s mRNA and protein in lung tissue of asthmatic mice

目的 研究烟草烟雾暴露对支气管哮喘 （简称哮喘）小鼠肺组织大麻素受体2（CB2）表达的影响,探讨吸烟加重哮喘气道炎症的相关机制。方法 雌性 SPF级 BALB/c纯系小白鼠40只,随机分为对照组、烟草烟雾暴露组、哮喘组、哮喘＋烟草烟雾暴露组,每组10只。建立哮喘小鼠模型和哮喘小鼠烟草烟雾暴露模型,采集支气管肺泡灌洗液 （BALF）行白细胞计数及分类,采用逆转录-聚合酶链式反应及 Westernblot检测各组小鼠气道 CB2受体 mRNA及蛋白的表达。结果 哮喘组、哮喘＋烟草烟雾暴露组 BALF中白细胞总数、嗜酸粒细胞、中性粒细胞均高 于对照组、烟草烟雾暴露组;哮喘＋烟草烟雾暴露组 BALF中白细胞总数和中性粒细胞均高于哮喘组（t=12.32、24.12,P 值均〈0.05）,嗜酸粒细胞低于哮喘组 （t=18.63,P =0.002）;哮喘组、哮喘＋烟草烟雾暴露组 CB2受体 mRNA及其蛋白表达水平均低于对照组、烟草烟雾暴露组,哮喘＋烟草烟雾暴露组明显低于哮喘组 （t=8.94、18.73,P 值均〈0.05）。结论 烟草烟雾暴露哮喘气道炎症以中性粒细胞为主,表现为中性粒细胞性哮喘;烟草烟雾暴露可通过抑制 CB2受体 mRNA及其蛋白表达,影响气道炎性细胞浸润,加重小鼠气道慢性炎症。

Objective To study the effect of tobacco smoke exposure on the expression of cannabinoid receptors 2 （CB2） in lung tissue of asthmatic mice, and discuss the mechanism of smoking aggravation of asthma airway inflammation. Methods Forty BALB/c iemalemice of SPF grade were randomly divided into control group, tobacco smoke exposure group, asthma group, asthma ＆ tobacco smoke exposure group, 10 in each group. Asthma mice model was established and the model of asthma mice were exposed to tobacco smoke, collecting bronchoalveolar lavage fluid （BAI.F） and detecting white blood cell count and classification, the reverse transcription polymerase chain reaction and Western blot imprinting method to detect the expressionof CB2 receptor＇s mRNA and protein. Results The total white blood cells, eosinophils, and neutrophils of BALF in asthma group, asthma ＆ tobacco smoke exposure group were higher than those in the control group and the tobacco smoke exposure group. The total white blood cells and neutrophils of BALF in asthma ＆ tobacco smoke exposure groupwere higher than those in the asthma group （ t =12.32,24.12, allP 〈0.05）,and the eosinophils were lower than the asthma group （t = 18.63, P =0.002）. CB2 receptor＇s mRNA and protein expression levels in asthma group and asthma ＆ tobacco smoke exposure group are lower than those in the control group and tobacco smoke exposure group, asthma ＆ tobacco smoke exposure was lower than those in asthma group （ t =8.94, 18.73, all P 〈0.05）. Conclusions Airway inflammation of tobacco smoke exposed asthma is dominated by neutrophils, showing neutrophilic asthma. Tobacco smoke exposure can curb the expression of CB2 receptor＇s mRNA and protein, which can affect the inflammatory cell infiltration of the airway and aggravate the chronic inflammation of airway in mice.