烟雾吸入伤大鼠肺组织细胞凋亡及凋亡调控基因表达的变化  

APOPTOSIS AND CHANGES IN APOTOSIS REGULATING GENES IN LUNG TISSUE CELLS AFTER SMOKE INHALATION INJURY IN RATS

作　　者：李文军[1] 杨宗城[2] 杨晓东[1] 李二红[1] 张斌[1] 张宏[1] 吉天鹏[1] 

机构地区：[1]解放军第159医院 [2]第三军医大学西南医院烧伤研究所

出　　处：《解放军医学杂志》2002年第2期142-144,T001,共4页Medical Journal of Chinese People's Liberation Army

摘　　要：探讨细胞凋亡及凋亡调控基因在大鼠烟雾吸入性损伤发生、发展中的作用及意义。以大鼠烟雾吸入伤为模型 ,应用TUNEL、免疫组化及RT PCR技术 ,观察烟雾吸入伤后不同时相肺组织中Bcl 2、Bax、Fas、Fas配体 (FasL)基因mRNA及蛋白的表达状态及其与细胞凋亡异常之间的关系。结果显示 ,烟雾吸入伤后细胞凋亡指数升高 ;烟雾吸入伤后可上调Bcl 2、Bax、Fas、FasL表达 ,mRNA表达在 12h达峰值 ,蛋白表达在 2 4h最高。在各时相点Bax、Fas、FasL基因表达与肺组织细胞凋亡有正相关关系。提示烟雾吸入伤后细胞凋亡增加 ,细胞存活同时受生存基因 (Bcl 2 )和死亡基因 (Bax、Fas、FasL)的双重调控 ,凋亡相关基因参与了烟雾吸入伤过程细胞凋亡的调控。To explore the role of apoptosis, apoptosis regulating genes in the pathogenesis and development of smoke inhalation injury. With smoke inhalation injury rat model, the changes int the expression of Bcl 2, Bax, Fas, FasL genes mRNA and protein contents and their relationship with apoptosis of lung tissue cells at different time points after the injury were observed with TUNEL, immunohistochemistry and RT PCR techniques. The results showed that: ①apoptosis indet of lung colls after smoke inhalation injury increased, ②expressions of Bcl 2, Bax, Fas, FasL genes were obviously up regulated in injury group, peaking at the 12th hour, whereas the peak of protein expression was at the 24th hour. Furthermore, a significant correlation was found between the expression of Fas, Fasl, Bax gene and apoptosis indices in lung cells. The results suggested that apoptosis participated in the early pathological process of smoke inhalation injury, and apoptosis regulating genes foot part in the regulation of apoptosis in smoke inhalation injury.

关 键 词：烟雾吸入性损伤 脱噬作用 Bcl-2基因 Bax基因 FAS基因 FASL基因 细胞凋亡 大鼠 肺组织 

分 类 号：R644[医药卫生—外科学] R563[医药卫生—临床医学]