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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, we observed that ozone (O3) had obvious cytotoxic effect on 3H-UdR-labeled airway epithelial cells cultured in vitro, and the degree of damage was positively correlated with O3 action time. The level of malondialdehyde (MDA) increased in O3-exposed group (P <0.01), which suggested that the mechanism of O3-induced injury was related to lipid peroxidation. Epidermal growth factor (EGF) could significantly reduce 3H release rate induced by O3 (P <0.01), reduce the cytotoxic index of O3 and intracellular MDA content (P <0.01) Have a protective effect. It was further observed that EOF at a concentration of 5 ng / ml abolished the decrease of intracellular reduced glutathione (GSH) and the increase of intracellular total glutathione (P <0.05), but they did not change the content of oxidized glutathione (GSSG) induced by O3 (P> 0.05), nor did they significantly increase the ratio of GSH / GSSG. All these suggested that the cytoprotection of EGF Mechanism may be related to its promotion of intracellular glutathione synthesis, while the conversion of GSSG GSH reduction process has no obvious effect.