Effect of sevoflurane on autophagy in lung tissues of asthmatic mice

Abstract

Objective To investigate the effect of sevoflurane on autophagy in lung tissues of asthmatic mice. Methods Twenty-four SPF female C57BL/6 mice, aged 6-8 weeks, weighing 23-27 g, were randomly divided into 3 groups (n=8 each) using a random number table: control group, asthma group and sevoflurane group.The mice were sensitized with intraperitoneal ovalbumin 10 μg and 1 mg potassium aluminium sulfate in 0.5 ml of normal saline (NS) on 1st day of establishment of the model, and asthma was challenged with aerosolized 1% ovalbumin in 50 ml of NS for 30 min once a day for 7 consecutive days starting from 15th day in asthma group.Asthma was induced using the method mentioned above, and the sensitized animals inhaled 3% sevoflurane for 1 h after each challenge in sevoflurane group.In control group, potassium aluminium sulfate 1 mg in 0.5 ml of NS was intraperitoneally injected on 1st day of establishment of the model, and the mice were exposed to aerosolized 0.9% NS 50 ml for 30 min once a day for 7 consecutive days starting from 15th day.At 24 h after the last challenge, the lung was lavaged, and broncho-alveolar lavage fluid (BALF) was collected for determination of the inflammatory cell count and concentrations of interleukin-13 (IL-13) and IL-10 in BALF (by enzyme-linked immunosorbent assay). The lung tissues were taken for examination of the inflammatory cell infiltration and damage to the bronchial epithelia and to the structure of alveolus and for determination of Beclin-1 and microtubule-associated protein 1 light chain 3 (LC3) expression (by Western blot). Results Compared with control group, the inflammatory cell count and concentrations of IL-13 and IL-10 in BALF were significantly increased, and the expression of Beclin-1 and LC3 in lung tissues was significantly up-regulated in asthma group (P<0.05). Compared with asthma group, the inflammatory cell count and concentrations of IL-13 in BALF were significantly decreased, the IL-10 concentration in BALF was significantly increased, and the expression of Beclin-1 and LC3 in lung tissues was significantly down-regulated in sevoflurane group (P<0.05). There was significantly less inflammatory cell infiltration in lung tissues, necrosis and shedding of bronchial epithelial cells and alveolar wall disruption in sevoflurane group. Conclusion The mechanism by which sevoflurane inhibits airway inflammation is related to inhibition of autophagy in asthmatic mice. Key words: Asthma; Anesthetics, inhalation; Autophagy; Lung