Expression of collagenase in mice with hyperoxia-induced acute lung injury
- VernacularTitle:间质胶原酶在高氧所致急性肺损伤中的表达
- Author:
Xiangfeng ZHANG
;
Cuangfa ZHU
;
Shuang LIU
;
D.foda HUSSEIN
- Publication Type:Journal Article
- Keywords:
Hyperoxia;
Acute lung injury after Matrix metalloproteinases(MMPs);
Interstitial collagenase
- From:
Chinese Journal of Emergency Medicine
2008;17(4):366-370
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of interstitial collagenase in the pathogenesis of acute lung injury induced by hyperoxia outside of sealed cages and breath room air,and to study the mechanism of The severity of lung injury.Methods Seventy-two C57BL/6 mice were divided into normal control group,hyperoxia for 24 hours group,hyperoxia for 48 hours and hyperoxia for 72 hours group randomly,18 mice in each group.The hyperoxia group exposedin sealed cages with＞95%oxygen,and the control group were put in the inspiratory room.The expression of interstitial collagenase mRNA and protein in lung tissues was studied by reverse transcript-polymerase chain reaction(RT-PCR)and immunohistochemistry.Results Hyperoxia caused acute lung injury in mice.by The expression of interstitial collagenase mRNA in lung tissues was increased after 24 hours of hyperoxia compared with their control group[0.59±0.11 vs 0.07±0.01,q=3.t5 P＜0.01],the expression was higher at 72 hours of hyperoxia(0.68±0.12,q=3.78 P＜0.01).Immunohistochemistry study showed interstitial collagenase protein was mainly expressed in cytoplasm of airway epithelial cells,while Ⅱ type alveolar epithelial cells mainly and vascular smooth muscle cells in hyperoxia mice.The expression of interstitial collagenase protein in airway epithelium significantly increased at 24 hours of hyperoxia compared with their control group[(28.54±9.60) vs (13.48±4.32)q=2.62 P＜0.05],and the expression level was lower after 48 and 72 hours of hyperoxia(20.32±5.68) vs, (15.24±4.65).Conclusion Hyperoxia cause acute lung injury in mice;interstitial collagenase play an important role in the development of hyperoxia-induced lung injury in mice.
