2006Chongqing Yike Daxue xuebaoRequires access

The expression change of aquaporin 1 in hyperoxic lung injury

Hao Jie

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Abstract

Objective:To study the expression change of aquaporin1 in hyperoxia-induced lung injury and the mechanism of action in lung oedema.Methods:Thirty-two juvenile(about two weeks) Wistar rats were randomly divided into breathing room-air group(n =8) and hyperoxia exposure group(n =8 at 3,7 and 14days respectively).The rats were continuously exposed to oxygen(O20.95)or room air(O2=0.21,respectively.The distributions of AQP1 in the lung tissues were detected by immunohistochemistry and their mRNA expressions were measured by RT-PCR.In addition,the wet-to-dry weight ratio(W/D),the protein content of bronchoalveolar lavage fluid(BALF),lung leak index,histological changes of hyperoxia-induced lung injury were measured respectively.Results:Light microscopic findings in the hyperoxia group including oedema,hemorrhage and extensive inflammatory cells in the lungs were observed.The lung W/D?the protein content in BALF and the lung leak index in hyperoxia group were significantly higher than those in room air group.The expressions of AQP1 mRNA in the lungs were significantly decreased at 3d of hyperoxia-exposure,minimized at 7d and increased from 14d(P0.05).Immunohistochemistry for AQP1 was seen primarily in microvascular endothelia cells around bronchus and alveolus,and interstitial cells;the positive regions were similar for room-air group and hyperoxia group.The dynamic changes of AQP1 protein level coincided with the changes of AQP1 mRNA expression.Conclusion:Hyperoxic lung injury may induce regulative unbalance of aquaporins expression,maybe it is one of the reasons for lung oedema caused by hyperoxic lung injury.

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Objective:To study the expression change of aquaporin1 in hyperoxia-induced lung injury and the mechanism of action in lung oedema.Methods:Thirty-two juvenile(about two weeks) Wistar rats were randomly divided into breathing room-air group(n =8) and hyperoxia exposure group(n =8 at 3,7 and 14days respectively).The rats were continuously exposed to oxygen(O20.95)or room air(O2=0.21,respectively.The distributions of AQP1 in the lung tissues were detected by immunohistochemistry and their mRNA expressions were measured by RT-PCR.In addition,the wet-to-dry weight ratio(W/D),the protein content of bronchoalveolar lavage fluid(BALF),lung leak index,histological changes of hyperoxia-induced lung injury were measured respectively.Results:Light microscopic findings in the hyperoxia group including oedema,hemorrhage and extensive inflammatory cells in the lungs were observed.The lung W/D?the protein content in BALF and the lung leak index in hyperoxia group were significantly higher than those in room air group.The expressions of AQP1 mRNA in the lungs were significantly decreased at 3d of hyperoxia-exposure,minimized at 7d and increased from 14d(P0.05).Immunohistochemistry for AQP1 was seen primarily in microvascular endothelia cells around bronchus and alveolus,and interstitial cells;the positive regions were similar for room-air group and hyperoxia group.The dynamic changes of AQP1 protein level coincided with the changes of AQP1 mRNA expression.Conclusion:Hyperoxic lung injury may induce regulative unbalance of aquaporins expression,maybe it is one of the reasons for lung oedema caused by hyperoxic lung injury.

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Available abstract

Objective:To study the expression change of aquaporin1 in hyperoxia-induced lung injury and the mechanism of action in lung oedema.Methods:Thirty-two juvenile(about two weeks) Wistar rats were randomly divided into breathing room-air group(n =8) and hyperoxia exposure group(n =8 at 3,7 and 14days respectively).The rats were continuously exposed to oxygen(O20.95)or room air(O2=0.21,respectively.The distributions of AQP1 in the lung tissues were detected by immunohistochemistry and their mRNA expressions were measured by RT-PCR.In addition,the wet-to-dry weight ratio(W/D),the protein content of bronchoalveolar lavage fluid(BALF),lung leak index,histological changes of hyperoxia-induced lung injury were measured respectively.Results:Light microscopic findings in the hyperoxia group including oedema,hemorrhage and extensive inflammatory cells in the lungs were observed.The lung W/D?the protein content in BALF and the lung leak index in hyperoxia group were significantly higher than those in room air group.The expressions of AQP1 mRNA in the lungs were significantly decreased at 3d of hyperoxia-exposure,minimized at 7d and increased from 14d(P0.05).Immunohistochemistry for AQP1 was seen primarily in microvascular endothelia cells around bronchus and alveolus,and interstitial cells;the positive regions were similar for room-air group and hyperoxia group.The dynamic changes of AQP1 protein level coincided with the changes of AQP1 mRNA expression.Conclusion:Hyperoxic lung injury may induce regulative unbalance of aquaporins expression,maybe it is one of the reasons for lung oedema caused by hyperoxic lung injury.

Key concepts: Hyperoxia, Lung, Aquaporin 1, Bronchoalveolar lavage, Immunohistochemistry, Pathology, Room air distribution, Medicine

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