高体积分数氧致慢性肺疾病早产鼠肺上皮细胞凋亡及其调控机制  

Apoptosis of Alveolar Epithelial Cell and Its Mechanism in Premature Rat with Hyperoxia-Induced Chronic Lung Disease

作　　者：岳晓红[1] 富建华[1] 薛辛东[1] 

机构地区：[1]中国医科大学附属盛京医院儿科,沈阳110004

出　　处：《实用儿科临床杂志》2008年第2期95-98,共4页Journal of Applied Clinical Pediatrics

基　　金：国家自然科学基金项目资助(30672253)

摘　　要：目的 探讨高体积分数氧致慢性肺疾病（CLD）早产鼠肺泡上皮细胞（AEC）凋亡的动态变化规律及Caspase-3 mRNA、Bax和Bcl-2基因的调控作用。方法 将60只早产SD鼠生后1d内随机分为高体积分数氧暴露组（高氧组）和空气组（对照组）各30只，制备高体积分数氧致CLD早产鼠模型，应用脱氧核苷酸末端转移酶介导的原位缺口末端标记（TUNEL）、反转录-聚合酶链反应（RT—PCR）技术及链霉亲和素-过氧化物酶复合物（SABC）免疫组织化学方法，检测生后1、3、7、14及21d AEC的凋亡指数（AI）和肺组织Caspase-3mRNA、Bax及Bcl-2基因蛋白的表达。相关分析采用Spearman分析。结果 与对照组比较，高氧组3dAEC的AI、肺组织Caspase-3 mRNA水平及Bax基因蛋白表达开始升高，7～21d明显增加，Caspase-3 mRNA水平在此期间持续于高水平；Bcl-2基因表达7d开始降低，14～21d明显降低。高氧组AEC的AI与肺组织Caspase-3 mRNA及Bax表达均呈正相关，与Bcl-2表达呈负相关。结论高体积分数氧可致CLD早产鼠肺组织Caspase-3 mRNA基因表达增强，使Bax和Bcl-2介导Bax／Bcl-2基因表达比例失衡，是CLD早产鼠肺上皮细胞凋亡的重要机制之一。Objective To explore the apoptosis of alveolar epithelial cell （ AEC ） and the dynamic changes of Caspase - 3 mRNA and Bax and Bcl - 2 expression in premature rat with hyperoxia - induced chronic lung disease （CLD）. Methods Sixty premature rats within 1 day af- ter birth were randomly divided into 2 groups ： hyperoxia group （ n = 30 ） and control group （ n = 30 ）. Hyperoxia - induced premature rat CLD models were prepared, and situ nick end - labeling （TUNEL） , reverse transcription polymerasechain reaction （ RT - PCR ） and immunohistochemical technique were used to determine apoptosis index（AI） of AEC and the expressions of Caspase -3 mRNA and Bax and Bcl -2 proteins in lung tissues at 1,3,7,14 and 21 d after birth. Results Compared with control group,in the hypcroxia group, on the third day after exposured to hyperoxia, the AI of AEC and the expressions of Caspase - 3 mRNA and Bax began to increase, and the expression of Caspase - 3 mRNA was kept at high level on 7 -21 d. The expression of Bcl- 2 began to decrease on 7 d,and significantly decreased on 7 -21 d. AI of AEC was positively correlated with the expression of Caspase - 3 mRNA and Bax, and negatively with the expression of Bcl - 2. Conclusions Hyperoxia may induce the increased expression of Caspase -3 mRNA ,which might result in the abnormal expression of Bax and Bcl -2 in lung tissues and their imbalance, which might be one of the underlying mechanisms of apoptosis of AEC in premature rats with CLD.

关 键 词：高体积分数氧 慢性肺疾病 细胞凋亡 含半胱氨酸的门冬氨酸特异水解酶 B细胞淋巴瘤/白血病-2相关X蛋白 B细胞淋巴瘤/白血病-2 

分 类 号：R722.6[医药卫生—儿科]