中国药理学通报Issue(6)：870-875,6.DOI:10.3969/j.issn.1001-1978.2015.06.026
姜黄素衍生物C085对K562细胞的作用及机制研究
Effects of curcumin derivatives C085 on K562 cells and its mechanism
摘要
Abstract
Aim To explore the anti-proliferation and apoptotic effects of C085, a curcumin derivative, on K562 cells and its mechanism. Methods MTT assay and flow cytometry were used to examine cell prolifera-tion and apoptosis, respectively. The phosphorylation levels of Bcr-Abl initiated signaling proteins were ana-lyzed using Western blot. Results The results showed that C085 suppressed the growth of K562 cells and the IC50 value was about 5-fold lower than that of Cur. C085 also induced significant apoptosis on K562 cells in 24 hours when compared with imatinib. Western blot results demonstrated that C085 down-regulated the phosphorylation of Bcr-Abl in K562 cells in a dose-de-pendent manner. The phosphorylation of Stat 5 and <br> Crkl, which were downstream signaling proteins of Bcr-Abl kinase, was also inhibited by C085. C085 caused the opening of mitochondrial PT holes as detected by JC-1 fluorescent, which inhibited Bcl-2 and enhanced Bax , then induced apoptosis. Conclusion C085 in-hibited BCR-ABL+ K562 cells through inhibiting BCR-ABL kinase activity and down-regulating its down-stream signal proteins. Directly acting on mitochondrial PT hole and then activating apoptosis- associated pro-teins are also involved in the pro-apoptotic effect of C085 .关键词
C085/姜黄素/IM/BCR-ABL/增殖/凋亡/机制Key words
C085/curcumin derivative/IM/BCR-ABL/proliferation/apoptosis/mechanism分类
医药卫生引用本文复制引用
吴莺,陈瑞家,吴丽贤,许建华..姜黄素衍生物C085对K562细胞的作用及机制研究[J].中国药理学通报,2015,(6):870-875,6.基金项目
福建省教育厅中青年教师资助项目(No JA13150) （No JA13150）
