高氧致CLD早产鼠肺上皮细胞凋亡及相关基因表达的动态研究  

Apoptosis of alveolar epithelial cell and expression of Bax and Bcl-2 in premature rat with chronic lung disease

作　　者：富建华[1] 薛辛东[1] 

机构地区：[1]中国医科大学附属第二医院儿科,辽宁沈阳110004

出　　处：《中国医科大学学报》2005年第2期100-101,104,共3页Journal of China Medical University

基　　金：辽宁省自然科学基金资助项目(20022071)

摘　　要：目的:探讨高氧致早产鼠慢性肺疾病(CLD)发生中肺泡上皮细胞(AEC)凋亡的动态变化规律及Bax和Bcl-2基因的调控作用.方法:将60例早产鼠随机分为实验组和对照组,制备高氧致早产鼠CLD模型,应用TUNEL及免疫组织化学技术,观察生后1,3,7,14,21 d AEC的凋亡指数(AI)和肺组织Bax及Bcl-2基因蛋白的表达强度.结果:实验组3 d AEC的AI明显升高(P＜0.01),7～21 d持续于高水平(P＜0.001);Bax基因蛋白表达3 d开始增加(P＜0.05),7～21 d明显增加(P＜0.01),Bcl-2基因表达7 d开始降低(P＜0.05),14～21 d明显降低(P＜0.01);实验组AI与Bax表达呈正相关(r=0.571,P＜0.05)、与Bcl-2表达呈负相关(r=-0.543,P＜0.05).结论:暴露高氧环境中早产鼠,由肺组织Bax及Bcl-2基因表达异常而介导的AEC程序性死亡机制参与了CLD的发生过程.Objective: To investigate the effect of hyperoxia on apoptosis of alveolar epithelial cell(AEC) and regulation of Bax and Bcl-2 expression in premature rat with chronic lung disease(CLD) .Methods:Sixty premature rats were randomly divided into 2 groups, model group(n=30) and control group(n=30). The apoptotic AEC was detected by using in situ nick end-labeling(TUNEL) technique, and expression of Bax and Bcl-2 in lung were detected by using immunohistochemisty stain. Results:The apoptotic index(AI) of AEC and the expression of Bax increased 3 days after hyperoxia, which reached the peak at the 7th to 21st day. The expression of Bcl-2 decreased from the 7th to 21st day. The AI of AEC was positively correlated with expression of Bax , and negatively with expression of Bcl-2.Conclusion:Apoptosis of AEC may play an important role in the genesis and progression of hyperoxia-induced CLD, which may be related with the abnormality expression of Bax and Bcl-2.

关 键 词：高氧 慢性肺疾病 细胞凋亡 BAX基因 BEL-2基因 

分 类 号：R722.1[医药卫生—儿科]