Expression Of Adenosine Receptor A1 In Chronic Obstructive Pulmonary Disease (COPD) Could Be Suppressed By Inhaled Corticosteroid And Anticholinergic Agents

Objectives: To investigate the expression of adenosine receptor A1 in pulmonary tissue of the rats model of COPD and observe the effects of inhaled corticosteroid or anticholinergic agent on its expression in order to explore the role of adenosine and its receptor in the pathogenesis of airway inflammation in COPD.Methods: A rat model of COPD was established by tobacco smoke inhalation. Thirty SD rats were randomly divided into control group,COPD group,COPD with inhaled corticosteroid (BUD) group and COPD with inhaled anticholinergic agent, ipratropium bromide (IAP) .The total number of cells and the percentages of polymorphonuclear leukocyte(PMN) in bronchalveolar lavage fluid (BALF) were counted.RT-PCR was used to determine the expression level of A1AR in lung tissue. Results: 1. The percentages of PMN in BALF in COPD were increasedsignificantly than those in BUD and IAP intervention group and control group(P<0.01). The percentages were still elevated in BUD/IAP intervention groups compared to those in control group,but no difference was found between BUD group and IAP group. 2.The expression level of A1AR in pulmonary tissue in COPD was higher than those in BUD/IAP intervention groups and control group (P<0.05) , while the expression level of A1AR in two intervention groups was not different significantly (P>0.05) . Conclusion: l.Tabocco smoke inhalation could copy COPD model in SD rats successfully.2.In the rats model of COPD the percentage of PMN in BALF was increased significantly . The expression level of A1AR in pulmonary tissue was increased also which exhibited a positive correlation with PMN counts, suspect adenosine takes an important role in COPD airway inflammation,it can provide a new target for COPD therapy.3.Corticosteroid suppressed airway inflammation of COPD characteristic of PMN infiltration.lt was supposed this effect was mediated by decreased expression of Al AR. 4.Anticholinergic agent also exhibited potency to suppress A1AR expression but the mechanism was unknown.