Objective: To evaluated the effect of curcumin on the bortezomib-resistant myeloma cells and the expression of Notch1 signaling pathway, in order to further explore its potential mechanism.
Methods: Curcumin, bortezomib, and curcumin combined bortezomib were added into RPMI 8266, U266, 5 nmol/L bortezomib-resistant RPMI 8266 (RPMI 8226-V5R), 5 nmol/L bortezomib-resistant U 266 (U266-V5R) and CD138+ plasma cells respectively. The cell proliferation was measured by MTT assay. the apoptotic rate was determined by flow cytometry, and the Western blot was used to detect the expression of apoptosis-related proteins. Then, the expression of Notch1 in cells was inhibited by notch1 inhibitor DAPT and RNA interference, the above-motioned experiments should be repeated.
Results: Compared with single drug-treated groups, the treatment with 2 drugs could further inhibit cell proliferation, induce apoptosis and enhance the inhibition effect on notch1 signaling pathway (P<0.05), while the inhibiting Notch1 signaling pathway could reduce cell proliferation and increase the expression of cleaved caspase-3.
Conclusion: Curcumin can increase chemosensitivity of myeloma cells to bortezomib, this effect may be related to the inhibition of Notch1.
题目: 姜黄素通过抑制Notch1信号通路增强多发性骨髓瘤对硼替佐米的化疗敏感性.
目的: 探讨姜黄素对耐硼替佐米的骨髓瘤细胞的作用以及对Notch1信号通路表达的影响，进一步探索其潜在的作用机制。.
方法: 分别将姜黄素、硼替佐米及姜黄素+硼替佐米作用于骨髓瘤细胞系RPMI8266、U266、耐5 nmol/L硼替佐米的RPMI 8266（RPMI8226-V5R）、耐5 nmol硼替佐米的U266（U266-V5R）及骨髓瘤CD138+浆细胞，应用MTT法检测细胞增殖活性，流式细胞术检测细胞凋亡，Western blot检测凋亡相关蛋白的表达；利用notch1抑制剂DAPT及RNA干扰技术抑制细胞内notch1表达，重复上述实验。.
结果: 与单药组相比，联合作用组可进一步抑制细胞增殖，增加细胞凋亡，增强对Notch1信号通路的抑制作用（P＜0.05）；而抑制Notch1可以减少细胞的增殖，并增加凋亡相关蛋白Cleaved caspase-3的表达水平。.
结论: 姜黄素能够增强骨髓瘤细胞对硼替佐米的敏感性，此作用可能与Notch1受抑制有关。.