中文摘要：

目的观察高体积分数氧（高氧）暴露下胎鼠肺泡Ⅱ型上皮细胞（AECⅡ）的线粒体DNA编码细胞色素氧化酶亚基Ⅰ、Ⅱ（COXⅠ、COXⅡ）mRNA表达的动态变化,探讨其在早产鼠高氧肺损伤发生发展的可能作用。方法分离、培养19 d胎鼠AECⅡ,经贴壁纯化后随机分为高氧组和空气组。高氧组在更换培养液后通入950 mL/L氧气及50 mL/L二氧化碳混合气,3 L/min,10 min后密封。2组均置于37℃、50 mL/L二氧化碳培养箱中培养。2组分别于高氧或空气暴露6、12、24 h提取AECⅡ总RNA,采用半定量反转录聚合酶链反应（RT-PCR）测定其COXⅠ和COXⅡmRNA表达。采用SPSS12.0软件进行统计学分析。结果与同时间点空气组比较,高氧暴露6、12 h时,COXⅠmRNA的表达显著升高（t=3.832 P=0.019,t=10.431 P=0）,其后下降,24 h时2组比较无显著性差异（t=0.360 P=0.731）。高氧暴露6 h时,COXⅡmRNA表达显著升高（t=2.795 P=0.035）,12、24 h时2组无显著差异（t=0.892 P=0.40,t=2.018 P=0.071）。结论高氧暴露诱导胎鼠AECⅡ中COXⅠmRNA和COXⅡmRNA表达上调,可能是高氧肺损伤的保护作用机制之一。

英文摘要：

Objective To observe the expression of mitochondrial encoding cytochrome oxidase subunit Ⅰ（ COX Ⅰ ） and subunit Ⅱ （ COX Ⅱ ） in type Ⅱ alveolar epithelial cell（ AEC Ⅱ ） of rats exposed to hyperoxia and explore the role of COX Ⅰand COX Ⅱ in hyperoxia - induced lung injury. Methods AEC Ⅱ were gained by primary culture from 19 - days fetal rats lung. After purified, AEC Ⅱwere randomly assigned to hyperoxia group and air group. Hyperoxia group was flushed the flake with 950 mL/L 02 and 50 mL/L CO2 at 3 L/min for 10 min, then sealed. Both groups were in CO2 culture chamber（37℃,50 mL/L CO2 ）. After 6,12 and 24 hours of exposure, AEC Ⅱ were harvested and extracted for total RNA. COX Ⅰand COX Ⅱ mRNA were detected by reverse transcription polymerase chain reaction（ RT - PCR）. The results were analyzed by SPSS 12.0 softwore. Results Compared with air group, COX ⅠmRNA expression in hyperoxia group increased significantly at 6 hours（t =3.832 P =0.019） and 12 hours（t =10.431 P=0） ,respectively,then decreased to the equivalent level in 24 hours （ t = 0. 360 P = 0.731 ）. Compared with air group, COX Ⅱ mRNA expression in hyperoxia group increased significantly at 6 hours （ t = 2. 795 P = 0. 035 ）, then decreased to the equivalent level at 12 hours （ t = 0. 892 P = 0.40） and 24 hours （ t = 2.018 P = 0.071 ）. Conclusions Exposure of hyperoxia up - regulate the expressions of COX Ⅰ mRNA and COX Ⅱ mRNA in AEC Ⅱ ,which may be a protective mechanism of hyperoxia - induced lung injury.