中文摘要：

目的探讨融合肽CTP-ODl和CTP—0132对伊马替尼（imatinib）敏感和耐药的慢性粒细胞白血病细胞株（K562、K562G01）的促凋亡生物学效应及其分子机制。方法将CTP—ODl、CTP—OD2融合肽分别处理K562和K562G01细胞，用瑞氏染色和DAPI染色检测两种细胞的凋亡形态学变化；westernblot检测凋亡相关蛋白Bcl-2、Bax及pBcr—Abl、pStat5、pCrkL变化。结果CTP—ODl和CTP．OD2处理K562和K562G01细胞后，胞浆出现空泡，细胞核碎裂，染色质浓缩、边缘化；westernblot结果表明，与阴性对照组相比，融合肽处理组Bax蛋白表达上调（P〈0．05），Bcl-2、pBcr-Abl、pStat5、pCrkL蛋白均表达减少（P均〈0．05）。结论CTP．ODI和CTP—OD2通过抑制Bcr．Abl激酶活性促进imatinib敏感株K562和耐药株K562G01细胞凋亡。

英文摘要：

Objective To evaluate the pro-apoptosis effect and molecular mechanism of fusion peptides CTP-OD1 and CTP-OD2 on imatinib-sensetive or -resistant chronic myeloid leukemia （CML） cell lines K562 and K562GO1. Methods K562 and K562G01 cells were respectively treated with fusion peptides CTP-OD1 and CTP-OD2,. Wright＇s and DAPI stainings were used to visualize the mor- phological features of cell apoptosis. Western blot was used to examine the levels of apoptotic related protein Bel-2, Bax, pBcr-Abl, pStat5 and pCrkL. Results After the treatment of CTP-ODland CTP-OD2, K562 and K562G01 ceils displayed typical features of ap- optosis, including cytoplasmic vacuolation, nuclear fragmentation, and condensation and marginalization of chromatin. The level of Bax was higher in the groups treated with CTP-OD1 and CTP-OD2 than that in control group （ P 〈 0.05 ）, while the levels of Bcl-2, pBcr- Abl, pStat5 and pCrkL were decreased （P 〈 0.05） in the groups treated with fusion peptides. Conclusion CTP-OD1 and CTP-OD2 could induce apoptosis of both imatinib-sensitive and -resistant CML cell lines by inhibiting Bcr-Abl kinase activity.