摘要
本研究观察到臭氧（Ｏ３）对体外培养经３Ｈ－ＵｄＲ标记的免气道上皮细胞有明显细胞毒性作用，且损伤程度与Ｏ３作用时间呈正相关。Ｏ３暴露组细胞内丙二醛（ＭＤＡ）产生增多（Ｐ＜０．０１），提示Ｏ３损伤细胞的机制与胞膜脂质过氧化有关。表皮生长因子（ＥＧＦ）可明显降低Ｏ３所致的３Ｈ释放率（Ｐ＜０．０１）、降低Ｏ３的细胞毒指数及细胞内ＭＤＡ含量（Ｐ＜０．０１），证明ＥＧＦ对气道上皮细胞有保护作用。进一步还观察到浓度为５ｎｇ／ｍｌ的ＥＯＦ可以取消Ｏ３所引起的细胞内还原型谷胱甘肽（ＧＳＨ）含量降低（Ｐ＜０．０１），并增加细胞内谷胱甘肽总含量（Ｐ＜０．０５），但不能改变Ｏ３所致的氧化型谷胱甘肽（ＧＳＳＧ）含量的增加（Ｐ＞０．０５），对ＧＳＨ／ＧＳＳＧ比值也无明显提高，这些都提示ＥＧＦ的细胞保护机理可能与其促进细胞内谷胱甘肽合成有关，而对ＧＳＳＧ转化为ＧＳＨ的还原过程影响不明显。
In this study, it was observed that ozone (O3) exposure has cytotoxic effects on cultured airway epithelial cells, which was positively related with exposure duration. Both the production of malondialdehyde (MDA) and the 3H release in the exposure group were much higher than the control (P<0.01), suggesting that lipOperoxidation occurring in the cell membrane was reponsible for the cellular injury observed under O3 attack. EGF at low concentration (5 ng/ml) showed cytoprotective effect on airway epithelial cells exposed to O3 as shown by attenuated MDA production and decrease of 3H release and cytotoxic index (P<0.01). Pretreatment with EGF could reverse the depletion of intracellular GSH content as a result of of exposure and increase the toeal glututhionein the cells. The above results suggest that the cytoprotection of EGF on airway epithelial cells may be related to its promotive effect on GSH synthesis.
出处
《生理学报》
CAS
CSCD
北大核心
1996年第2期190-194,共5页
Acta Physiologica Sinica
基金
国家自然科学基金
关键词
气道上皮细胞
臭氧
表皮生长因子
细胞保护
airway epithelial cells
ozone
epidermal growth factor
cytoprotection
glutathione
malondialdehyde
