摘要
本研究在臭氧（Ｏ３）对培养的兔支气管上皮细胞损伤模型上观察了热应激处理对支气管上皮细胞抗Ｏ３损伤的保护效应，并初步探讨其机制。结果表明，４２℃热应激处理３０ｍｉｎ可明显降低Ｏ３攻击下的细胞毒指数（ＣＩ）及细胞内ＭＤＡ含量，表示热应激对支气管上皮细胞具有细胞保护作用。进一步观察表明，热应激预处理可增加细胞内还原型谷胱甘肽（ＧＳＨ）含量、降低氧化型谷胱甘肽（ＧＳＳＧ）含量、增加ＧＳＨ／ＧＳＳＧ比值，并能增加两型谷胱甘肽的总量。结果提示热应激的细胞保护作用机理可能与其增加从谷胱甘肽合成及增强谷胱甘肽还原酶活性，提高细胞自身的内源性抗氧化能力有关。
A model of injury on cultured rabbit bronchial epithelial cells induced by exposure to ozone (O 3 ) was made in order to study the cytoprotective effect of heat stress. The results showed that there were high cytotoxic index (CI) ( P <0.01) and increased intracellular malondialdehyde (MDA) content ( P <0.01) in comparison with the control .Pretreatment with heat (42℃,30 mins) significantly reduced MDA and CI in bronchial epithelial cells exposed to O 3 ( P <0.01),indicating that heat stress had cytoprotective effect on bronchial epithelial cells. Futhermore study showed that GSH was increased whereas GSSG reduced ( P <0.05) and the ratio of GSH/GSSG and the total content of glutathione were increased in heat stress ( P <0.05).It is suggested that the mechanism of cytoprotective effect of heat stress may be related to increasing the synthesis of total glutathione and elevating the activity of glutathione reductase.
出处
《中国应用生理学杂志》
CAS
CSCD
1996年第3期243-246,共4页
Chinese Journal of Applied Physiology
基金
国家自然科学基金
