Expression of M3 acetylcholine receptor in asthmatic mice and bronchial airway remodeling prediction

Abstract

ABSTRACT. This study aimed to investigate the role of M 3 acetylcholine receptor (M 3 -AChR) expression in airway remodeling. Additionally, we aimed to evaluate the effects of ipratropium bromide solution inhaled in an early phase of asthma on airway remodeling in ovalbumin (OVA)-sensitized and challenged mice. Thirty BALB/c mice were divided into three groups, namely, control group (saline sensitized/challenged mice), asthma group (OVA sensitized/challenged mice), and treatment group (OVA sensitized/challenged mice treated by ipratropium bromide). Pathological changes were detected by histological staining in the bronchopulmonary tissue of mice. WAt/ Pbm (the airway wall area /basement membrane perimeter) ratio of the asthma group (25.37 ± 4.25) increased significantly (P < 0.05) when compared with that of the control (12.89 ± 1.71) and treatment group (15.82 ± 2.91). WAm/Pbm (smooth muscle wall area / basement membrane perimeter) ratio of the asthma group (7.58 ± 2.16) increased significantly (P < 0.05) when compared with that of the control (2.55 ± 0.72) and treatment group (3.36 ± 1.69). M 3 -AChR concentration increased in the treatment group (29.24 ± 3.59) and was significantly different (P < 0.05) from that of the control group (25.50 ± 1.83). During asthma treatment, SAMA can alleviate airway remodeling in murine model by lessening the thickness of bronchial walls and inhibiting the proliferation of smooth muscle cells. There were no obvious changes in M 3 -AChR density in the murine model of asthma characterized by airway remodeling. However, ipratropium bromide may up-regulate the expression of M 3 -AChR in bronchial walls of asthmatic murine model.

Effect of Tiotropium Bromide on Airway Inflammation and Programmed Cell Death 5 in a Mouse Model of Ovalbumin-Induced Allergic Asthma

“…Holownia et al [38] found that tiotropium could increase cytosolic ChRM3 protein level in induced sputum cells of COPD patients. Similarly, ipratropium bromide, another common acetylcholine receptor antagonist, could upregulate ChRM3 expression in bronchial walls of an asthmatic murine model [39]. The results of existing studies are inconsistent.…”