【摘要】 目的:探讨高氧对早产鼠Ⅱ型肺泡上皮细胞(typeIIalveolarepithelialcells,AECⅡ)转分化的影响。方法:原代培养早产大鼠的AECⅡ,建立高氧细胞损伤模型。利用倒置相差显微镜和透射电镜观察细胞的形态变化。用免疫细胞化学染色法检测AECⅡ特异性肺泡表面活性蛋白-C(surfactantproteinC,SP-C)及Ⅰ型肺泡上皮细胞(typeⅠalveolarepitheli-alcells,AECⅠ)特异性水通道蛋白5(aquaporin5,AQP5)的表达。用RT-PCR和流式细胞术分别检测SP-C、AQP5mRNA及蛋白的表达。结果:随着给氧时间的延长,原代培养的AECⅡ伸展变平,失去其板层体及微绒毛,丧失AECⅡ的特性,获得AECⅠ样外观。伴随其形态学改变,AECⅡ逐渐停止表达其特异性蛋白SP-C,开始表达AECⅠ特异性蛋白AQP5。高氧组给O2后24、48及72h,SP-CmRNA、SP-C+细胞的表达率及荧光指数(fluorescenceindex,FI)较同时间点的空气组明显降低,AQP5的上述指标在24h和48h则较空气组明显增加。高氧组给O2后72h,AQP5的表达开始减弱,与同时间点的空气组相比较无明显差异。结论:高氧诱导的早产大鼠AECⅡ转分化在肺泡上皮细胞损伤的修复中起重要作用。更多还原

【Abstract】 AIM: To investigate the effect of hyperoxia on the transdifferentiation of type II alveolar epithelial cells (AECII) in premature delivery rats. METHODS: AECII from fetal rat lung were cultured primarily to establish a model of cells damaged by hyperoxia. The morphological changes of the cells were observed by inverted phase contrast microscope and transmission electron microscope. AECII-specific surfactant protein C (SP-C) and AECI-specific aquaporin 5 (AQP5) were detected by immunocytochemical staining. The expression levels of SP-C, AQP5 mRNAs and their protein were detected by RT-PCR and flow cytometry. RESULTS: With the time of exposure to hyperoxia, primarily cultured AECII spread and flattened, losing lamellar bodies and microvilli. They rapidly lost their characteristics and gained some AECI appearance. With their morphological changes, AECII stopped expressing AECII-specific protein SP-C but began expressing AECI-associated protein AQP5. Compared with exposure to air at the same time in air group for 24, 48 and 72 hours, the expression rate of SP-C mRNA in positive cells and fluorescence index (FI) decreased markedly in 3 groups, but compared with exposare to air for 24 and 48 hours the expression of AQP5 increased significantly in 2 groups. The expression of AQP5 began decreasing and showed no marked difference compared with air group at the same time of for 72 hours. CONCLUSION: The transdifferentiation of AECII induced by hyperoxia may play a key role in the repaire of alveolar epithelial cell injury in premature delivery rats.更多还原