Flavopiridol联合Bortezomib对多发性骨髓瘤的细胞增殖抑制作用

目的探讨细胞蛋白激酶抑制剂Flavopiridol及蛋白酶抑制剂Bortezomib在体内抑制多发性骨髓瘤细胞U266的细胞增殖作用及其机制。方法以不同浓度的Flavopiridol及Bortezomib分别、联合作用于U266细胞,用MTT法检测细胞增殖抑制作用。采用western blot法检测Bcl-2及Mcl-1表达变化;结果①Flavopiridol比Borte-zomib对U266细胞增殖抑制作用更强,IC50值分别为52.5nM,25nM。②与单独用药相比,Flavopiridol联合Borte-zomib作用于U266细胞,IC50值有明显的下降为17.5nM。③Flavopiridol及Bortezomib给药前后,Bcl-2蛋白表达无变化,而Mcl-1蛋白表达明显下降。结论 Flavopiridol联合Bortezomib用药能在体内明显抑制多发性骨髓瘤细胞U266的生长,其机制主要是通过诱导细胞凋亡来抑制增殖。

The inhibitory effect of Flavopiridol in combination with bortezomib on the proliferation of multiple myeloma

Objective To discuss the protein kinase inhibitor Flavopiridol and proteasome inhibitor Bortezomi inhibi- tion of multiple myeloma cells U266 cell proliferation and its mechanism of action. Methods different concentrations of Flavopiridol and /or Bortezomib,respectively,the effects of U266 cells proliferation was detected by MTT. By western blot to detect the expression of Bcl-2 and Mcl-1, rearch the change of Bcl-xl, Mcl-1 while U266 was dealed with Fla- vopiridol and Bortezomib. Results ①Compared with Bortezomib and Flavopiridol more proliferation of U266 cells, （IC50：52.5 nM,25 nM）. ②Compared with the drug alone,Flavopiridol and Bortezomib,while the role of U266 cells with IC50 values significantly reduced（IC50： 17.5 nM）. ③Flavopiridol and Bortezomib before and after administration, the Bel-2 protein expression remained unchanged,while Mcl 1 protein expression was significantly decreased. Conclusion Flavopiridol and Bortezomib medication in the body significantly inhibited U266 growth of multiple myeloma cells, and its mechanism is mainly inhibition of proliferation by inducing apoptosis.