^(60)Coγ射线照射对肺泡Ⅱ型细胞和肺泡隔间质细胞的生物效应  

Biological effect of ^(60)Coγ ray on alveolar type Ⅱ cells and interstitial cells of alveoliar septum in radiation pulmonary injury

作　　者：刁瑞英[1] 宋良文[1] 王少霞[1] 李明[1] 

机构地区：[1]军事医学科学院放射与辐射医学研究所病理学研究室,北京100850

出　　处：《细胞与分子免疫学杂志》2008年第2期119-121,共3页Chinese Journal of Cellular and Molecular Immunology

基　　金：国家自然科学基金资助项目(30570545)

摘　　要：目的:探讨60Coγ射线照射对肺泡II型细胞和肺泡隔间质细胞的生物效应。方法:原代分离肺内II型上皮细胞(AT-Ⅱ)和间质细胞包括巨噬细胞和成纤维细胞,分别进行0、3、5、7Gy的γ射线照射,用细胞核嗜银染色观察照射对AT-Ⅱ增殖的影响;用酶谱分析检测照射后AT-Ⅱ和间质细胞培养上清中基质金属蛋白酶-2、-9(MMP-2,-9)的活性;用ELISA检测间质细胞培养上清中TGF-β1和IV型胶原含量。结果:AT-Ⅱ的核仁数量随照射剂量增加而增多,其中7Gy组最高;AT-II培养上清中MMP-2、-9活性随照射剂量增加呈先增高后降低趋势,间质细胞上清中MMP-2、-9活性和TGF-β1水平逐渐升高,IV型胶原分泌水平呈先降低后升高趋势。结论:放射性肺损伤早期,AT-Ⅱ、巨噬细胞和成纤维细胞均参与肺组织无效性重建过程,与晚期肺纤维化启动有一定的内在联系。AIM： To explore the biological effect of ^60Coγ ray on alveolar type Ⅱ cells and interstitial cells of alveoliar septum. METHODS： Alveolar type Ⅱ cells（AT-Ⅱ） and interstitial cells including interstitial macrophages and fibroblasts were irradiated by 0, 3, 5, 7 Gy of γ ray respectively. The effect of irradiation on AT-Ⅱ proliferation was observed by argentation against nucleus. The activity of MMP-2, -9 in supematants from AT-Ⅱ and interstitial cells after irradiation was determined by zymography. The levels of TGF-β1 and collagen type Ⅳ in supematant from interstitial cells after irradiation were measured by ELISA. RESULTS： The nucleolus number of AT-Ⅱ was increased with the increase of irradiation dose and group 7 Gy reached the highest level. The activity of MMP-2, -9 in supernatant from AT-Ⅱ after irradiation increased at first and then decreased gradually. The activity of MMP-2, -9 and the content of TGF-β1 in interstitial cells increased step by step, but collagen type Ⅳ decreased at first and then increased. CONCLUSION： AT-Ⅱ, macrophages and fibroblasts are all involved in pulmonary invalid remodeling course in early radiation pulmonary injuory, which is related to the initiation of pulmonary fibrosis in late period.

关 键 词：肺泡Ⅱ型上皮细胞 间质细胞 MMPS TGF-Β1 Ⅳ型胶原 

分 类 号：R392.3[医药卫生—免疫学]