摘要
目的探讨绿脓杆菌致急性肺损伤小鼠的ATF3表达规律及意义。方法以荧光标记的绿脓杆菌(PA)(滴度1.5×108CFU/ml) 50μl经鼻滴入C57BL/6野生型小鼠气管构建急性肺损伤模型,通过肺泡灌洗液(BALF)中的蛋白含量、肺组织干湿比测定肺微血管通透性和肺水肿程度变化;采用组织切片和HE染色观察肺组织病理变化; qRT-PCR检测ATF3在野生型急性肺损伤小鼠肺组织中的表达规律。结果经鼻滴入绿脓杆菌后导致肺微血管通透性增加和肺水肿加重,小鼠肺组织呈典型急性肺损伤病理改变,结果支持成功构建了经鼻滴入绿脓杆菌致ALI模型。ATF3表达于正常小鼠肺组织,经鼻滴入绿脓杆菌后小鼠肺组织中ATF3 mRNA的表达于0、3、6、12 h及24 h时相点分别为1.006±0.136,9.954±0.624,4.578±1.463,2.342±0.122,3.249±0.680,其中在3 h时相点达最高峰,随之逐渐下降,于24 h时相点基本能回到正常水平。结论 ATF3作为负性调控因子对绿脓杆菌致急性肺损伤小鼠有一定保护作用。
Objective To investigate the expression and significance of ATF3 in Pseudomonasaeruginosa-induced acute lung injury. Methods Acute lung injury model was established in C57BL/ 6 wild-type mice by nasal instillation of fluorescent-labeled Pseudomonas aeruginosa (PA) ( titer 1.5×10^8CFU/ ml)50 μl. The changes of lung microvascular permeability and pulmonary edema were measured by the proteincontent in BALF and the ratio of dry to wet of lung tissue. The expression of ATF3 in lung tissue of wild-typeacute lung injury mice was detected by qRT-PCR. Results After intranasal drip of Pseudomonas aeruginosa(PA), pulmonary microvascular permeability increased and pulmonary edema aggravated. The lung tissue ofmice showed typical pathological changes of acute lung injury. The results supported the successfulestablishment of the ALI model induced by intranasal drip of Pseudomonas aeruginosa (PA). The expression ofATF3 mRNA in lung tissues of normal mice was observed at 0, 3, 6, 12, and 24 h after intranasal drip ofPseudomonas aeruginosa. The expression of ATF3 mRNA in lung tissues of mice reached its peak at 3 h, thendecreased gradually, and reduced to normal at 24 h. This suggest that ATF3 was involved in stress. ConclusionAs a negative regulatory factor ATF3 has a protective effect on Pseudomonas aeruginosa induced acute lung injury in mice.
作者
吴秀琳
陈光春
李明霞
郭亮
吴学玲
Wu Xiulin;Chen Guangchun;Li Mingxia;Guo Liang;Wu Xueling(Department of geriatrics,XinanHospital,Army medical university,Chongqing 400038,China;Department of chest surgery,Daping Hospital,Army medical university,Chongqing 400042,China;Central laboratory,Chongqing Armed Police ForceHospital,Chongqing 400016,China;Department of Respiratory,Xinqiao Hospital,Army medical university,Chongqing 400037,China;Department of Respiratory,Renji Hospital,Shanghai Jiaotong University School ofMedicine,Shanghai 200127,China)
出处
《中华肺部疾病杂志(电子版)》
CAS
2018年第5期538-543,共6页
Chinese Journal of Lung Diseases(Electronic Edition)
基金
国家自然科学基金资助项目(81270130)