目的：吸入高浓度氧气是导致新生早产儿肺发育障碍,并最终发展为慢性肺疾病(CLD)的主要原因,但其详细机制尚不清楚。本文旨在确定肺泡Ⅱ型上皮细胞(AECⅡ)凋亡在高氧诱导的早产鼠CLD形成中的作用及其主要信号机制。方法：93只新生早产大鼠随机分为两组:对照组(n= 45)吸入空气,模型组(n= 48)吸入≥95%氧气。分别采用原位末端标记技术(TUNEL)、电镜及逆转录聚合酶链反应(RT PCR)技术检测特定时间点各组大鼠肺组织细胞凋亡及其相关因子的表达。结果：模型组凋亡指数(AI)自7d起明显高于对照组(P<0. 05),发生凋亡的细胞是AECⅡ;模型组BaxmRNA3d起高于对照组(P<0. 05),Bcl 2自7d起低于对照组(P<0. 05);两组FasmRNA表达无差异(P>0. 05)。结论：早产大鼠CLD过程中存在AECⅡ凋亡,这可能是导致高氧诱导的CLD早产大鼠肺泡发育障碍的主要因素之一;凋亡信号的启动可能有Bax与Bcl 2比值变化的参与,而与Fas的转录表达无关。

OBJECTIVE: Exposure to high concentrations of oxygen may impair the pulmonary development in premature neonates and ultimately result in chronic lung disease (CLD). But its precise mechanism has not been identified. This study aimed to investigate the role of alveolar epithelial type Ⅱ cells (AECⅡ) apoptosis and its signaling pathways in the development of hyperoxia-induced CLD in premature rats. METHODS: Ninety-three premature newborn rats were randomly assigned into a Control group (exposed to air,n = 45) and a Model group (exposed to ≥95% O_2,n = 48). Apoptosis and relative factor expression were determined with the terminal deoxynucleotidyl transferase-mediated nick end labelling (TUNEL), electron microscopy, and reverse transcriptase PCR (RT-PCR). RESULTS: The apoptotic index increased in the Model group from day 7 to day 21 of hyperoxia inducement(P <0.05). The apoptotic cells were AECⅡ. Bax mRNA levels in the Model group were higher than those in the Control group after the 3rd day(P <0.05), while Bcl-2 expression in the Model group was lower on the 7th, 14th and 21st days than that in the Control group(P <0.05). There was no difference in the Fas mRNA expression between the two groups. CONCLUSIONS: Apoptosis of AECⅡis present in the process of hyperoxia-induced CLD and may be one of major causes of poor alveoli development related to hyperoxia-induced CLD . The changes in the Bax and Bcl-2 ratio may be involved in the initiation of the signaling pathway of AECⅡapoptosis, while Fas transcriptional expression may be irrelevant.