title: Expression of M3 acetylcholine receptor in asthmatic mice and bronchial airway remodeling prediction.
abstract: This study aimed to investigate the role of M3 acetylcholine receptor (M3-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). M3-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 M3-AChR density in the murine model of asthma characterized by airway remodeling. However, ipratropium bromide may up-regulate the expression of M3-AChR in bronchial walls of asthmatic murine model.
authors.affiliation: Laboratory of Medicine, The Second Affiliated Hospital of Jilin University, Changchun, Jilin, China.
authors.forename: F
authors.initials: F
authors.lastname: Zhao
authors.affiliation: Department of Respiratory Medicine, The Second Affiliated Hospital of Jilin University, Changchun, Jilin, China.
authors.forename: J
authors.initials: J
authors.lastname: Yang
authors.affiliation: Department of Pediatrics, The Second Affiliated Hospital of Jilin University, Changchun, Jilin, China.
authors.forename: P
authors.initials: P
authors.lastname: Chen
authors.affiliation: Department of Respiratory Medicine, The Second Affiliated Hospital of Jilin University, Changchun, Jilin, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Respiratory Medicine, The Second Affiliated Hospital of Jilin University, Changchun, Jilin, China.
authors.forename: H
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Respiratory Medicine, The Second Affiliated Hospital of Jilin University, Changchun, Jilin, China.
authors.forename: Q
authors.initials: Q
authors.lastname: Zhang
mesh_terms: D056151:Airway Remodeling; D000818:Animals; D018927:Anti-Asthmatic Agents / Q000494:pharmacology / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D001980:Bronchi / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D005260:Female; D009241:Ipratropium / Q000494:pharmacology / Q000627:therapeutic use; D051379:Mice; D008807:Mice, Inbred BALB C; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000378:metabolism; D011950:Receptors, Cholinergic / Q000235:genetics / Q000378:metabolism*
chemical_list: D018927:Anti-Asthmatic Agents; D011950:Receptors, Cholinergic; D009241:Ipratropium