芹黄素通过抗氧化作用减轻阿霉素对正常血细胞的损伤

Apigenin Protects Normal Blood Cells Against Adriamycin-Induced Injury Depending on Antioxidative Action

本研究探讨芹黄素(apigenin,Api)对化疗药阿霉素损伤正常血细胞的保护作用及其机制。用MTT法测定芹黄素、阿霉素以及芹黄素联合应用阿霉素对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(ROS)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。结果显示,阿霉素培养1h后添加芹黄素继续培养至48h,未能明显影响阿霉素对K562细胞的增殖抑制作用,但阿霉素对PMN的细胞增殖抑制率明显下降。两药联合实验组与阿霉素组相比,PMN和K562细胞裂解上清液中的ROS和MDA水平均明显降低,SOD和GSH-Px活性均明显升高;而细胞裂解上清液中的氧化应激指标变化趋势于。上述实验结果表明芹黄素在不影响阿霉素抗白血病细胞增值的同时对正常血细胞具有保护作用,其可能机制是芹黄素提高了正常细胞内抗氧化物酶活性,同时降低氧化产物含量,减轻了阿霉素的氧化应激损伤副作用。

The objective of this study was to investigate the protection by apigenin （Api） against adriamycin - induced injury and its underlying mechanisms in normal blood cells. The proliferation inhibiting effect of apigenin, adriamyein or apigenin combined with adriamyein on K562 cells and polymorphonuclear leukocytes （PMNs） was 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 examined with speetrophotometrie method in the K562 cells and PMNs. The results indicated that the proliferation inhibiting effect of adriarnvcin （for 48 h） on K562 cells was not re-dueed by the addition of apigenin after adriamyein for 1 h. However, such inhibiting effect of adriamycin on PMNs was reversed by apigenin. As compared with the adriamycin group, the levels of ROS and MDA markedly decreased, while the activity of SOD and GSH - Px markedly increased both in K562 cells and PMNs by apigenin. It is concluded that apigenin protects normal blood cells against adriamyein -induced oxidative damage while maintaining the proliferation inhibi- ting effect of leukemia cells. The underlying mechanism may be involved that apigenin elevates activity of antioxidant en- zymes and meanwh/le decreases level of oxidative products so as to reducing adriamycin - induced oxidative stress injuries in normal blood ceils.