摘要
目的探讨去甲斑蝥素(NCTD)对人多发性骨髓瘤U266细胞Notch信号通路表达的影响。方法体外培养骨髓瘤U266细胞,不同浓度(10、20、40、80μmol/L)NCTD与U266细胞共同孵育后,采用CCK-8法检测细胞增殖抑制率;采用流式细胞术检测细胞凋亡率;采用qRT-PCR、Western blotting法检测细胞Notch2、Hes1、Cyclin D1和P21基因蛋白的表达。结果 20、40、80μmol/L NCTD能抑制U266细胞增殖,诱导细胞凋亡,其抑制效应具有时间和浓度依赖性;NCTD可上调瘤细胞中Notch2和P21基因蛋白的表达,同时降低Hes1和Cyclin D1表达。结论 NCTD能够抑制骨髓瘤细胞增殖,且能诱导细胞凋亡;细胞凋亡的发生可能与Notch信号通路中Notch2、P21表达上调,Cyclin D1和Hes1的表达下调有关。
Objective To investigate the effects of norcantharidin（NCTD） on the expression of Notch signal pathway in multiple myeloma U226 cells.Methods U226 cells were co-cultured with NCTD at various concentrations in vitro.The proliferation inhibition was measured with CCK-8 test.The cell apoptosis rate was analyzed with flow cytometry.The mRNA and protein expressions of Notch2,Hes1,Cyclin D1 and P21 in U266 cells were detected with qRT-PCR and Western blotting.Results NCTD could inhibit the proliferation of U266 cells and induce the apoptosis of cells in a time-and concentration-dependent manner.The mRNA and protein expressions（Notch2,P21） elevated with increased concentration of NCTD,while the expression of Hes1 and Cyclin D1 decreased.Conclusion NCTD can inhibit the proliferation and induce the apoptosis of U266 cells,which may be related to the up-regulation of Notch2 and P21,and the down-regulation of Cyclin D1 and Hes1.
出处
《山东大学学报（医学版）》
CAS
北大核心
2017年第3期32-37,共6页
Journal of Shandong University:Health Sciences
基金
贵州省科学技术基金项目(TJ2014-4)
贵阳市白云区科技基金项目(白科合同2014年度6号)
