Zhao F, Yang J, Chen P, Wang Y, Zhang H, Zhang Q
Laboratory of Medicine, The Second Affiliated Hospital of Jilin University, Changchun, Jilin, China.
Department of Respiratory Medicine, The Second Affiliated Hospital of Jilin University, Changchun, Jilin, China.
Genet Mol Res. 2016 Jul 15;15(3):gmr8805. doi: 10.4238/gmr.15038805.
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.
本研究旨在探讨M3型乙酰胆碱受体（M3-AChR）表达在气道重塑中的作用。此外，我们旨在评估在哮喘早期吸入异丙托溴铵溶液对卵清蛋白（OVA）致敏和激发小鼠气道重塑的影响。将30只BALB/c小鼠分为三组，即对照组（生理盐水致敏/激发小鼠）、哮喘组（OVA致敏/激发小鼠）和治疗组（用异丙托溴铵治疗的OVA致敏/激发小鼠）。通过组织学染色检测小鼠支气管肺组织的病理变化。哮喘组的气道壁面积/基底膜周长（WAt/Pbm）比值（25.37±4.25）与对照组（12.89±1.71）和治疗组（15.82±2.91）相比显著增加（P<0.05）。哮喘组的平滑肌壁面积/基底膜周长（WAm/Pbm）比值（7.58±2.16）与对照组（2.55±0.72）和治疗组（3.36±1.69）相比显著增加（P<0.05）。治疗组的M3-AChR浓度升高（29.24±3.59），与对照组（25.50±1.83）相比有显著差异（P<0.05）。在哮喘治疗期间，短效抗胆碱能药物（SAMA）可通过减轻支气管壁厚度和抑制平滑肌细胞增殖来减轻小鼠模型中的气道重塑。在以气道重塑为特征的哮喘小鼠模型中，M3-AChR密度无明显变化。然而，异丙托溴铵可能上调哮喘小鼠模型支气管壁中M3-AChR的表达。
