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Objective: To study the expression of AQP-1, AQP-3, AQP-4 and AQP-5 in the pulmonary tissues of mice with acute lung injury (ALI) induced by lipopolysaccharide (LPS) and to clarify the relationship of ALI with the expression of AQP-1, AQP-3, AQP-4 and AQP-5. Methods: Forty healthy male C57BL/6 mice were evenly randomized into 5 groups: LPS 4 h group, LPS 6 h group, LPS 8 h group, LPS 10 h group and control group. ALI model was induced with LPS in all the LPS groups. Real-time PCR was used to observe the expression changes of AQP-1, AQP-3, AQP-4 and AQP-5 mRNA. Immunohistochemical method and Western blotting assay were used to determine the changes of AQP-1, AQP-3, AQP-4 and AQP-5 protein in the pulmonary tissues of all the animals. Meanwhile, measurement of lung wet/dry (W/D) weight ratio and pathological staining were performed in each group. Results: The W/D values of the LPS 4 h, 6 h, 8 h and 10 h groups (4.39±0.19,4.58± 0.17,4.87±0.21 and 5.28±0.16, respectively) were significantly higher than that of the control group (3.99±0.25, all P<0.05). The expression of AQP-1 and AQP-5 protein in the lung of the LPS 4 h group decreased to (74.1±5.2)% and (70.3±7.1)% that of the control group; the expression of AQP-1 and AQP-5 protein in the lung of the LPS 8 h group decreased to (45.2±4.4)% and (38.6±8.9)% that of the control group, and the expression of AQP-3 and AQP-4 had no obvious changes. Conclusion: AQP-1 and AQP-5 may play important roles in the abnormal ALI fluid transportation and might be associated with the development of pulmonary edema. AQP-3 and AQP-4 may not participate in the development of pulmonary edema during ALI.

Objective: To investigate the expression of aquaporin 5 (AQP5) and MUC5AC in lung of bronchial asthmatic murine model and the regulatory effect of dexamethasone on the expression. Methods: Forty-eight female C57BL/6 mice were evenly randomized into control group, asthma group and dexamethasone group. The pathological changes of the lungs and the wet/dry weight ratios of the lungs were determined in mice of each group. The expression of AQP5 and MUC5AC mRNA in the lung was determined by real-time poly-merase chain reaction (real-time PCR); the AQP5 protein was examined by Western blotting assay; the distribution of AQP5 protein in the pulmonary tissue was studied immunohistochemically; and the content of MUC5AC in the bronchial alveolar lavage fluid (BALF) was determined by ELISA. Results: Compared with the control group, the pulmonary expression of AQP5 in asthma group was obviously decreased (mRNA by[42.5 ± 3.6]%, protein by [64.3 ± 8.2]%), while the expression of MUC5AC was increased (mRNA by[93.3±8.1]%,protein by[98.3%±7.2]%). Dexamethasone significantly decreased the pulmonary expression of AQP5 and MUC5AC compared with the asthma group (P<0.05). Conclusion: The decreased pulmonary expression of AQP5 in asthmatic mice might be related to the elevation of MUC5AC expression in the airway; dexamethasone can decrease AQP5 expression and therefore alleviate the overproduction of airway mucus, pulmonary inflammation and lung edema.

Objective: To investigate the expression of aquaporin 5 (AQP5) and MUC5AC in lung of bronchial asthmatic murine model and the regulatory effect of dexamethasone on the expression. Methods: Forty-eight female C57BL/6 mice were evenly randomized into control group, asthma group and dexamethasone group. The pathological changes of the lungs and the wet/dry weight ratios of the lungs were determined in mice of each group. The expression of AQP5 and MUC5AC mRNA in the lung was determined by real-time poly-merase chain reaction (real-time PCR); the AQP5 protein was examined by Western blotting assay; the distribution of AQP5 protein in the pulmonary tissue was studied immunohistochemically; and the content of MUC5AC in the bronchial alveolar lavage fluid (BALF) was determined by ELISA. Results: Compared with the control group, the pulmonary expression of AQP5 in asthma group was obviously decreased (mRNA by[42.5 ± 3.6]%, protein by [64.3 ± 8.2]%), while the expression of MUC5AC was increased (mRNA by[93.3±8.1]%,protein by[98.3%±7.2]%). Dexamethasone significantly decreased the pulmonary expression of AQP5 and MUC5AC compared with the asthma group (P<0.05). Conclusion: The decreased pulmonary expression of AQP5 in asthmatic mice might be related to the elevation of MUC5AC expression in the airway; dexamethasone can decrease AQP5 expression and therefore alleviate the overproduction of airway mucus, pulmonary inflammation and lung edema.

Objective: To study the expression of AQP-1, AQP-3, AQP-4 and AQP-5 in the pulmonary tissues of mice with acute lung injury (ALI) induced by lipopolysaccharide (LPS) and to clarify the relationship of ALI with the expression of AQP-1, AQP-3, AQP-4 and AQP-5. Methods: Forty healthy male C57BL/6 mice were evenly randomized into 5 groups: LPS 4 h group, LPS 6 h group, LPS 8 h group, LPS 10 h group and control group. ALI model was induced with LPS in all the LPS groups. Real-time PCR was used to observe the expression changes of AQP-1, AQP-3, AQP-4 and AQP-5 mRNA. Immunohistochemical method and Western blotting assay were used to determine the changes of AQP-1, AQP-3, AQP-4 and AQP-5 protein in the pulmonary tissues of all the animals. Meanwhile, measurement of lung wet/dry (W/D) weight ratio and pathological staining were performed in each group. Results: The W/D values of the LPS 4 h, 6 h, 8 h and 10 h groups (4.39±0.19,4.58± 0.17,4.87±0.21 and 5.28±0.16, respectively) were significantly higher than that of the control group (3.99±0.25, all P<0.05). The expression of AQP-1 and AQP-5 protein in the lung of the LPS 4 h group decreased to (74.1±5.2)% and (70.3±7.1)% that of the control group; the expression of AQP-1 and AQP-5 protein in the lung of the LPS 8 h group decreased to (45.2±4.4)% and (38.6±8.9)% that of the control group, and the expression of AQP-3 and AQP-4 had no obvious changes. Conclusion: AQP-1 and AQP-5 may play important roles in the abnormal ALI fluid transportation and might be associated with the development of pulmonary edema. AQP-3 and AQP-4 may not participate in the development of pulmonary edema during ALI.

Objective: To study the expression of AQP-1, AQP-3, AQP-4 and AQP-5 in the pulmonary tissues of mice with acute lung injury (ALI) induced by lipopolysaccharide (LPS) and to clarify the relationship of ALI with the expression of AQP-1, AQP-3, AQP-4 and AQP-5. Methods: Forty healthy male C57BL/6 mice were evenly randomized into 5 groups: LPS 4 h group, LPS 6 h group, LPS 8 h group, LPS 10 h group and control group. ALI model was induced with LPS in all the LPS groups. Real-time PCR was used to observe the expression changes of AQP-1, AQP-3, AQP-4 and AQP-5 mRNA. Immunohistochemical method and Western blotting assay were used to determine the changes of AQP-1, AQP-3, AQP-4 and AQP-5 protein in the pulmonary tissues of all the animals. Meanwhile, measurement of lung wet/dry (W/D) weight ratio and pathological staining were performed in each group. Results: The W/D values of the LPS 4 h, 6 h, 8 h and 10 h groups (4.39±0.19,4.58± 0.17,4.87±0.21 and 5.28±0.16, respectively) were significantly higher than that of the control group (3.99±0.25, all P<0.05). The expression of AQP-1 and AQP-5 protein in the lung of the LPS 4 h group decreased to (74.1±5.2)% and (70.3±7.1)% that of the control group; the expression of AQP-1 and AQP-5 protein in the lung of the LPS 8 h group decreased to (45.2±4.4)% and (38.6±8.9)% that of the control group, and the expression of AQP-3 and AQP-4 had no obvious changes. Conclusion: AQP-1 and AQP-5 may play important roles in the abnormal ALI fluid transportation and might be associated with the development of pulmonary edema. AQP-3 and AQP-4 may not participate in the development of pulmonary edema during ALI.

Objective: To investigate the expression of aquaporin 5 (AQP5) and MUC5AC in lung of bronchial asthmatic murine model and the regulatory effect of dexamethasone on the expression. Methods: Forty-eight female C57BL/6 mice were evenly randomized into control group, asthma group and dexamethasone group. The pathological changes of the lungs and the wet/dry weight ratios of the lungs were determined in mice of each group. The expression of AQP5 and MUC5AC mRNA in the lung was determined by real-time poly-merase chain reaction (real-time PCR); the AQP5 protein was examined by Western blotting assay; the distribution of AQP5 protein in the pulmonary tissue was studied immunohistochemically; and the content of MUC5AC in the bronchial alveolar lavage fluid (BALF) was determined by ELISA. Results: Compared with the control group, the pulmonary expression of AQP5 in asthma group was obviously decreased (mRNA by[42.5 ± 3.6]%, protein by [64.3 ± 8.2]%), while the expression of MUC5AC was increased (mRNA by[93.3±8.1]%,protein by[98.3%±7.2]%). Dexamethasone significantly decreased the pulmonary expression of AQP5 and MUC5AC compared with the asthma group (P<0.05). Conclusion: The decreased pulmonary expression of AQP5 in asthmatic mice might be related to the elevation of MUC5AC expression in the airway; dexamethasone can decrease AQP5 expression and therefore alleviate the overproduction of airway mucus, pulmonary inflammation and lung edema.