姜黄素诱导人慢粒白血病K562细胞凋亡与线粒体途径的关系

Induction of apoptosis by curcumin in K562 cells involves mitochondrion pathway

目的研究姜黄素（Cur）对慢性粒细胞白血病（CML）细胞株K562的作用，并且探讨该作用与线粒体凋亡途径的关系。方法应用MTT法检测Cur对细胞增殖的影响，AO／EB荧光染色法、细胞光度术、DNA凝胶电泳等方法观察细胞凋亡，分光光度法检测Caspase-3的活性，用蛋白免疫印迹法检测细胞色素C的含量。结果Cur对K562细胞抑制作用呈量效、时效关系；Cur对人正常骨髓单个核细胞与K562细胞之间有一定的选择性，对K562细胞的敏感性约为人正常骨髓单个核细胞的5倍，在对K562细胞抑制超过95％时，对人正常骨髓有核细胞几无毒性。Cur5．0，10．00g／mL作用24h，可诱导K562细胞凋亡，促进细胞色素C释放，激活caspase-3。结论Cur可通过线粒体途径诱导人慢性粒细胞白血病K562细胞凋亡。

Objective To test effects of curcumin （Cur） on K562 cells, and reveal the relationship between Cur-induced apoptosis and mitochondrion pathway. Methods MTI was used to examine the proliferation inhibited by Cur. The typical morphological changes of apoptosis were observed by AO/EB examined by fluorescence microscopy. Quantitate apoptotic cells with subdiploid DNA content was measured by flow cytometry. The activities of Caspase-3 were analyzed by spectrophotometry. The amounts of cytochrome C in cytosolic and S-100 fraction were tested by Western blot. Results Cur was a potent inhibitor of proliferation of K562 cells with low toxicity to normal marrow mononuclear cells. Cur induced cytosolic accumulation of cytochrome c and activities of caspase-3, triggering apoptosis of K562 cells. Conclusions Cur was able to induce the apoptosis of K562 cells by mitochondrion pathway.