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Effects of a Leukotriene Receptor Antagonist on Airway Remodeling in Asthmatic Mice via the Wnt/β -catenin Signaling Pathway / 中国医科大学学报
Journal of China Medical University ; (12): 226-230, 2018.
Article in Chinese | WPRIM | ID: wpr-704995
ABSTRACT
Objective To investigate the expression of Wnt7b, β -catenin, and c-Myc in asthmatic mice and the intervention of the leukotriene receptor antagonist montelukast on airway remodeling. Methods The asthma model was established by ovalbumin (OVA) induction. HE staining was used to observe the pathological changes in lung tissue. Serum OVA-sIgE levels were determined by ELISA. The level of Wnt7b, β -catenin, and c-Myc protein and mRNA in the lung tissue of mice was analyzed by Western blotting and real-time PCR. The basement membrane perimeter (PBM), wall area of bronchial tube (WAt), wall area of bronchial smooth muscle (WAm), and the number of smooth muscle cells were measured using medical image analysis software and standardized based on the PBM. Results The amount of OVA-slgE in the asthma group was significantly higher than in the control and montelukast groups (P < 0. 05). Western blotting and real-time PCR showed that the expression of Wnt7b, β -catenin, and c-Myc in the asthma group was higher than the expression in the control and montelukast groups (P < 0. 05). Image analysis showed that the WAt/PBM and WAm/PBM ratios in the montelukast group were significantly lower than those in the asthma group (P < 0. 05). Conclusion The Wnt/ β -catenin signaling pathway may be an important factor in the pathogenesis of asthma; montelukast may attenuate airway remodeling in asthmatic patients by decreasing the expression of Wnt7b, β -catenin, and c-Myc.

Full text: Available Index: WPRIM (Western Pacific) Type of study: Prognostic study Language: Chinese Journal: Journal of China Medical University Year: 2018 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Type of study: Prognostic study Language: Chinese Journal: Journal of China Medical University Year: 2018 Type: Article