吸入性损伤对小鼠肺组织细胞凋亡的影响  

The influence of smoke inhalation injury on the apoptosis of lung tissue cells in rats

作　　者：廖圣德[1] 赵烨德[1] 刘刚[1] 李旭东[1] 

机构地区：[1]解放军第四一一医院烧伤整形科,上海200081

出　　处：《中华航海医学与高气压医学杂志》2006年第2期102-104,共3页Chinese Journal of Nautical Medicine and Hyperbaric Medicine

摘　　要：目的探讨细胞凋亡、促凋亡基因和凋亡抑制基因在吸入性损伤发生的作用及意义。方法以小鼠烟雾吸入性损伤为模型,应用RT-PCR和TUNEL技术,观察其损伤后肺组织中Bcl-2和 Bax基因mRNA表达及细胞凋亡的变化。结果小鼠烟雾吸入性损伤后肺组织Bcl-2和Bax的表达增加,细胞凋亡指数升高,与对照组相比,差异有非常显著性(P<0．01)。结论提示细胞凋亡可能参与了吸入性损伤肺组织的病理形成过程。Objective To explore the role and significance of apoptosis, pro-apoptotic genes and apuptosis suppressor genes in the pathogenesis and development of inhalation injury. Methods Smoke inhalation injury model was established in rats, and the mRNA expressions of Bcl-2, Bax, and apoptosis in the lung tissue were observed. Results The expressions of Bcl-2 and Bax, and the apoptotic index （AI） in the inhalation injury group were significantly increased, compared with the control group （P 〈0.01 ）. Conclusions It is suggested that apoptosis might play an role in the pathology process of smoke inhalation injury.

关 键 词：吸入性损伤 细胞凋亡 BCL-2基因 BAX基因 

分 类 号：R83[医药卫生—航空、航天与航海医学]