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作 者:冯颖倩[1] 左学兰[1] 李瑞芳[1] 张克俭[1] 陈飞[1] 肖晖[1]
机构地区:[1]武汉大学中南医院血液科,湖北武汉430071
出 处:《中国实验血液学杂志》2008年第4期790-793,共4页Journal of Experimental Hematology
摘 要:本研究探讨柚皮素对化疗药阿霉素损伤的正常血细胞的保护作用。用MTT法测定柚皮素、阿霉素以及柚皮素联合阿霉素(Post1小时组、Post24小时组)应用对K562细胞和正常人外周血多形核白细胞(PMN)的增殖抑制作用,用分光光度法检测正常人外周血PMN和K562细胞裂解上清液中的活性氧(RO S)和丙二醛(MDA)的水平、超氧化物歧化酶(SOD)、谷胱苷肽过氧化物酶(GSH-Px)活性。结果表明:两药联合实验组(Post1小时组、Post24小时组)中,柚皮素无明显降低阿霉素对K562细胞的增殖抑制作用。Post1小时实验组与阿霉素组相比,PMN细胞裂解上清液中的活性氧(RO S)和丙二醛(MDA)水平明显降低,超氧化物歧化酶(SOD)和谷胱苷肽过氧化物酶(GSH-Px)活性则明显升高;而K562细胞裂解上清液中的氧化应激指标无明显变化。结论:柚皮素对阿霉素损伤的正常血细胞具有保护作用,其可能机制是柚皮素提高细胞内抗氧化物酶活性同时降低氧化产物含量。The objective of this study was to investigate the protection by naringenin against doxorubicin-induced oxidative damage in normal blood cells. Inhibiting effects of naringenin, doxorubicin and naringenin combined with doxorubieind on K562 cells and polymorphonuclear leukocytes were detected with MTT method, the level of reactive oxygen species (ROS) and lipid peroxidation (MDA), the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were examineded with spectrophotometric method in the K562 cells and polymorphonuclear leukocytes. The results indicated that the proliferation of K562 cells was not inhibited by the cytotoxicity of doxorubicin in combination of naringenin with doxorubicin. As compared with the doxorubicin, the addition of naringenin after doxorubicin for 1 hour, the levels of reactive oxygen species (ROS) and lipid peroxidation (MDA) obviously decreased, the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) obviously increased in the polymorphonuclear leukocytes, but these were not changed obviously in K562 cells. It is concluded naringenin can protect against doxorubicin-induced oxidative damage in normal blood cells. The mechanism of naringenin may be elevating activities of antioxidant enzyme and degrading oxidative production level in normal blood cells, and meanswhile decreasing level of oxidative products.
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