Objective To observe the effects of vitamin A combined with glucocorticoid on the structure and function of airway epithelium in asthmatic mice. Methods Sixty specific pathogen-free female C57bl/6 mice (6 to 8 weeks old) were randomized equally into control group, asthma group, dexamethasone (Dex) group, vitamin A (VA) group, and dexamethasone plus vitamin A (D+VA) group. Except for those in the control group, all the mice were stimulated repeatedly with house dust mites to establish asthma models. At 30 min before the last 3 stimulations, the mice in Dex group were intraperitoneally injected with 200 μL of dexamethasone. The mice in VA group were given vitamin A-rich food for 10 consecutive days starting on 21 days after the modeling. The mice in D+VA group received both dexamethasone treatment and vitamin A feeding, and the control mice were injected with 0.9% NaCl only. Within 24 h after the last challenge, invasive lung function test was performed to assess airway hyperresponsiveness (AHR) of the mice, bronchoalveolar lavage fluid (BALF) was collected from the mice for cell counting, and the trachea and lungs were sampled for pathological examination with HE staining. The expression of E-cadherin, caspase 3 and cleaved caspase 3 in the lung tissue were detected using immunohistochemical staining and Western blotting. Results Dexamethasone treatment aggravated airway epithelial injury in the asthmatic mice and obviously lowered the expression of E-cadhein (P < 0.05) and increased the expression of caspase 3 and cleaved caspase 3 in the lung tissues(P < 0.01). The asthmatic mice receiving vitamin A treatment showed significantly lowered AHR(P < 0.05), but their cell counts in the BALF and lung pathologies were similar with those in dexamethasone-treated mice. Compared with the mice with dexamethasone treatment, the mice receiving both dexamethasone and vitamin A treatment had significantly lowered AHR(P < 0.01), lessened airway epithelial injury, lowered expression levels of caspase 3 and cleaved caspase 3(P < 0.01) and increased expression of E-cadherin in the lung tissues(P < 0.01). Conclusion Dexamethasone promotes apoptosis of airway epithelial cells in asthmatic mice to aggravate airway epithelial injury. Vitamin A combined with dexamethasone can better reduce AHR and inhibit airway epithelial cell apoptosis to maintain the structural and functional integrity of the airway epithelium in asthmatic mice.
