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采用体外实验向大鼠肺匀浆或线粒体通入吸烟烟气的方法，研究了吸烟烟气致大鼠肺匀浆和线粒体脂质过氧化及茶多酚的拮抗作用。结果表明向肺匀浆或线粒体通入烟气后，随着通烟气时间的延长，肺匀浆或线粒体脂质过氧化物（ＬＰＯ）含量显著增加；通入烟气１．０ｍｉｎ后，随着温育时间的延长，肺匀浆ＬＰＯ含量也显著增加。说明吸烟烟气能够导致大鼠肺匀浆和线粒体脂质过氧化。预先向肺匀浆或线粒体中加入茶多酚（０．１ｍｇ／ｍｌ），结果显示茶多酚对吸烟烟气致大鼠肺匀浆或线粒体脂质过氧化具有显著的拮抗作用
In vitro experiments to rat lung homogenates or mitochondria access to smoking flue gas, smoking smoke induced lung homogenates and mitochondrial lipid peroxidation and tea polyphenols antagonistic effect. The results showed that the lung homogenate or mitochondrial lipid peroxide (LPO) content increased significantly with the passage of flue gas, Longer incubation time, lung homogenate LPO content also increased significantly. Smoking smoke can cause lung homogenates and mitochondrial lipid peroxidation in rats. Pre-added to the lung homogenate or mitochondria of tea polyphenols (0.1mg / ml), the results show that tea polyphenols on cigarette smoke induced lung homogenate or mitochondrial lipid peroxidation has a significant antagonistic effect