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Study on mechanism of bronchial epithelial cell apoptosis in acute lung injury induced by smoke inhalation of mouse model by epithelial cell apoptosis markers detection

Author: 
Zhengjun Cui, Imran Khan, Xiaobo Wang, Jialin Sun, Rongqiang Yang and Qing-nan Meng
Subject Area: 
Health Sciences
Abstract: 

Background: The modern medical studies clarify that, it is apoptosis, not the necrosis which is actively involved in Acute Lung Injury (ALI) caused by smoke inhalation. A variety of lung apoptosis namely vascular endothelial cells, pulmonary inflammatory cells and alveolar type II cells transpire in such state. The apoptic cell population among them certainly jacked within few hours then sustained a high level.in addition, apoptic genes namely Bcl-2 and Bax was also changed in mRNA and protein expression level were materially increased. The aspiration of our dissertation is to investigate the mechanism of apoptosis induced by smoke inhalation in bronchial epithelium. Objective: To find out the Mechanism Of Bronchial Epithelial Cell Apoptosis In Acute Lung Injury Induced By Smoke Inhalation Of Mouse Model By Epithelial Cell Apoptosis Markers Detection. Methods: Twenty-two Wild-type C57BL/6 mice were subjected to smoke inhalation to formulate model after random classification into 4 groups: Control group (not exposed, n =4), 2m (exposed to smoke for 2minutes, n=6), 3m (exposed to smoke for 3minutes, n=6), 4m (exposed to smoke for 4minutes, n=6). 24hrs after the smoke exposure 10% chloral hydrate solution 350mg/kg according to body weight were administrated by intra-peritoneal injection. All the mice were sacrificed step by step at a 24hrs, 48hrs and 72hrs time interval. After anaesthesia, 1ml fresh blood was collected from the left ventricle of the mice, henceforth opening the thoracic cavity. The left lung was obtained to execute the histo-pathological investigation and grading. To reveal apoptosis and its mechanism, in situ western bloat and TUNEL were accomplished after getting the sample of bronchial epithelial cell collected from the different lobes of right lung. Results: Contrast with control group, haemorrhage, wall thickening, inflammation and oedema were clearly evident in lung tissue histo-pathological examination of 2m group, 3m group and 4m group. Moreover, positive expression of NF-kB, CASPASE- 3 and PARP were perceived. Conclusions: Bronchial epithelial cell apoptosis has a significant role in acute lung injury due to fume inhalation was evident. Positive expression of NF-kB, CASPASE- 3 and PARP indicated their involvements in acute lung injury.

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