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目的 研究姜黄素 (Cur)对慢性粒细胞白血病 (CML)细胞株K5 62增殖的影响 ,并且探讨这种影响与P2 10 bcr/abl及其激活的Ras信号途径的关系。方法 应用MTT法检测Cur对细胞增殖的影响 ,应用Westernblot的方法检测蛋白含量的变化。结果 Cur对P2 10 bcr/abl阳性的K5 62细胞抑制作用呈量效、时效关系 ,Cur 10mg·L-1作用 48h对K5 62细胞的抑制率高达 (81 9± 1 0 ) % ;相比之下 ,已知对P2 10 bcr/abl无影响的VP 16作为抗癌药对照 ,对K5 62细胞的抑制作用明显较弱。Cur和VP 16对K5 62细胞的不同作用提示Cur对K5 62细胞作用可能有特异性 ,而这个特异的作用靶点可能就是引起CML对多种化疗药物耐药的CML特征性的P2 10 bcr/abl蛋白。Westernblot的实验结果表明Cur使K5 62细胞P2 10 bcr/abl、MEK 1和c Jun蛋白含量明显减少 ,且呈量效关系 ,相比之下 ,VP 16对K5 62细胞P2 10 bcr/abl的蛋白含量无影响而仅轻微减少MEK 1和c Jun的蛋白含量 ,提示MEK 1和c Jun蛋白含量的减少是非特异性的 ,并且 ,在P2 10 bcr/abl阳性的K5 62细胞 ,Cur除了非特异性地抑制细胞中MEK 1及c Jun的表达外 ,Cur还可能通过特异性地抑制K5 62细胞的特异性靶点P2 10 bcr/abl的表达 ,从而下调其下游的Ras信号途径中的其它信号分子。结论 Cur可特
Objective To study the effect of curcumin on the proliferation of chronic myeloid leukemia (CML) cell line K5 62 and to explore the relationship between this effect and P2 10 bcr/abl and its activated Ras signaling pathway. Methods The effect of Cur on cell proliferation was detected by MTT assay. The protein content was detected by Western blot. Results The curative effect of Cur on K562 cells with P2 10 bcr/abl positive was dose-effect and time-dependent. The inhibition rate of Cur 10 mg·L-1 for 48 h on K562 cells was as high as (81 9± 1 0) %. Under the control of VP16, which is known to have no effect on P2 10 bcr/abl, as an anti-cancer drug, its inhibitory effect on K562 cells was significantly weaker. The different roles of Cur and VP 16 on K562 cells suggest that Cur may have specificity for K5 62 cells, and this specific target may be the CML characteristic P2 10 bcr/ that causes CML resistance to various chemotherapeutic agents. Abl protein. The results of Westernblot showed that Cur reduced the protein levels of P2 10 bcr/abl, MEK1, and c Jun in K562 cells in a dose-dependent manner. In contrast, the protein of VP 16 on P2 10 bcr/abl in K562 cells. The content had no effect but only slightly decreased the protein content of MEK 1 and c Jun, suggesting that the reduction of the protein content of MEK 1 and c Jun was non-specific, and that in the K562 cells positive for P 2 10 bcr/abl, Cur was non-specifically In addition to inhibiting the expression of MEK 1 and c Jun in cells, Cur may also specifically down-regulate the expression of specific target P2 10 bcr/abl in K5 62 cells, thereby down-regulating other signaling molecules in the downstream Ras signaling pathway. Conclusion Cur