摘要
目的探讨海水吸入型肺损伤中自噬过程,以及地塞米松对其干预作用。方法 40只大鼠完全随机分为正常对照组、1、3、6、12 h海水处理组,每组8只。采用气管内滴注海水(3 ml/kg)的方法制作海水吸入型急性肺损伤大鼠模型,观察病理变化,检测肺组织湿干比,western blot检测beclin-1的表达变化。体外实验A549细胞分为正常对照组、12 h海水组、地塞米松+12 h海水组、3-MA+12 h海水组,采用western blot检测beclin-1和bax的表达变化。结果海水吸入后,大鼠肺部严重损伤,水肿明显,beclin-1随损伤时间延长表达量增加,在海水处理后12 h达到高峰。体外实验中海水刺激增加了beclin-1和bax的表达,然而与海水组相比,地塞米松预处理增加了beclin-1的表达,同时使bax的表达下降。3-MA预处理则效果相反。结论自噬参与了海水吸入型肺损伤的修复过程,地塞米松能够通过加强自噬并且抑制凋亡减轻肺损伤。
Objective To observe the process of autophagy in seawater aspiration-induced acute lung injury and the intervention effect of dexamethasone.Methods 40 rats were randomly divided into 5 groups：normal control group,1 h,3 h,6 h,and 12 h seawater group.Every group contains 8 rats.Seawater aspiration-induced acute lung injury model was made by seawater instillation （3 ml/kg） into the airway.Pathological changes and lungs＇wet/dry ratio were carried out after modeling.The expression of beclin-1 was measured by western blot.A549 cells were divided into 4 groups：normal control group,12 h seawater group,dexamethasone ＋ 12 h seawater group,3-MA ＋ 12 h seawater group.The expression of beclin-1 and bax was measured by western blot.Results After seawater stimulation,manifestations of lung injury and edema were obvious.The expression of beclin-1 was up-regulated along with the extension of time and reached the peak at 12 h after seawater aspiration.In cells experiment,seawater stimulation increased the expression of beclin-1 and bax.However,pre-treatment of dexamethasone increased the expression of beclin-1 and attenuated the expression of bax compared with seawater group.Furthermore,3-MA had an opposite effect with dexamethasone.Conclusion Autophagy plays an important part in the repairmen of seawater aspirationinduced acute lung injury.Dexamethasone attenuated lung injury by enhancing autophagy and inhibiting apoptosis.
出处
《中华肺部疾病杂志（电子版）》
CAS
2014年第6期15-18,共4页
Chinese Journal of Lung Diseases(Electronic Edition)
基金
国家自然科学基金(81270124)
关键词
急性肺损伤
海水
地塞米松
自噬
细胞凋亡
Acute lung injury
Seawater
Dexamethasone
Autophagy
Cell apoptosis
