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

Abstract

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 femalemice 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 (BALF) 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, all P<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. Key words: Tobacco smoke exposure; Bronchial asthma; Cannabinoid receptors 2