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

[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 m RNA 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.[Method] Twenty-two Wild-type C57BL/6 mice were subjected to smoke inhalation to prepare model after random classification into 4 groups: Control group(not exposed,n =4),2min(exposed to smoke for 2minutes,n=6),3min(exposed to smoke for 3minutes,n=6),4min(exposed to smoke for 4minutes,n=6).24 hours 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 24 hrs,48hrs and 72 hrs 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 blot and TUNEL were performed after getting the sample of bronchial epithelial cell collected from the different lobes of right lung.[Result] Contrast with control group,haemorrhage,wall thickening,inflammation and oedema were clearly evident in lung tissue histo-pathological examination of 2min group,3min group and 4min group.Moreover,positive expression of NF-k B,CASPASE-3 and PARP were observed.[Conclusions] The important role of bronchial epithelial cell apoptosis in acute lung injury due to fume inhalation was evident.