Li-ping Tan1, Feng Xu, Feng-wu Kuang. 1. Intensive Care Unit, Children's Hospital, Chongqing University of Medical Science, Chongqing 400014, China.
Abstract
OBJECTIVE: To explore the expression and the modulation of aquaporin 5(AQP5) in hyperoxia induced lung injury. METHODS: Sixty four Wistar rats of 2 weeks old, were randomly assigned to following groups (n=8): air group, hyperoxia 3, 7, 14 days groups, air + dexamethasone (Dex), hyperoxia 3, 7, 14 days + Dex groups. The rats were kept in oxygen chamber at normal pressure (O(2)> or =95%) in hyperoxia groups, and in normal pressure air (O(2)=21%) in room-air group, and the rats in Dex groups were injected with Dex (5 mg.kg(-1).d(-1)) intraperitoneally for 3 consecutive days in room-air or hyperoxia exposure. The expression of AQP5 mRNA level and the location were detected by reverse transcription-polymerase chain reaction and immunohistochemistry respectively. RESULTS: AQP5 was strongly labeled in alveolar epithelial type I cells, and was also expressed in the secretory epithelium plasma membrane in the airway. The location of AQP5 in hyperoxia groups was not changed, but the expression of AQP5 mRNA had a notable gradual decline when the time of hyperoxia exposure was prolonged, compared to control group (all P<0.05). There was no difference in AQP5 mRNA level between hyperoxia groups and hyperoxia + Dex groups at different time points (all P<0.05). CONCLUSION: The significant decrease in AQP5 may be an important factor of pulmonary edema formation in hyperoxia-induced lung injury. Dex does not have effect on modulating the AQP5 expression in acute lung injury.
OBJECTIVE: To explore the expression and the modulation of aquaporin 5(AQP5) in hyperoxia induced lung injury. METHODS: Sixty four Wistar rats of 2 weeks old, were randomly assigned to following groups (n=8): air group, hyperoxia 3, 7, 14 days groups, air + dexamethasone (Dex), hyperoxia 3, 7, 14 days + Dex groups. The rats were kept in oxygen chamber at normal pressure (O(2)> or =95%) in hyperoxia groups, and in normal pressure air (O(2)=21%) in room-air group, and the rats in Dex groups were injected with Dex (5 mg.kg(-1).d(-1)) intraperitoneally for 3 consecutive days in room-air or hyperoxia exposure. The expression of AQP5 mRNA level and the location were detected by reverse transcription-polymerase chain reaction and immunohistochemistry respectively. RESULTS:AQP5 was strongly labeled in alveolar epithelial type I cells, and was also expressed in the secretory epithelium plasma membrane in the airway. The location of AQP5 in hyperoxia groups was not changed, but the expression of AQP5 mRNA had a notable gradual decline when the time of hyperoxia exposure was prolonged, compared to control group (all P<0.05). There was no difference in AQP5 mRNA level between hyperoxia groups and hyperoxia + Dex groups at different time points (all P<0.05). CONCLUSION: The significant decrease in AQP5 may be an important factor of pulmonary edema formation in hyperoxia-induced lung injury. Dex does not have effect on modulating the AQP5 expression in acute lung injury.