| 摘要: |
| 目的探讨桔梗皂甙D（platycodin，PD）与伊马替尼（imatinib，IM）联合用药抑制慢性粒细胞白血病细胞株K562的作用及机制研究。方法体外培养CML细胞株K562，CCK-8测定PD和IM单药及联合用药对K562细胞增殖的抑制作用；流式细胞仪检测AnnexinV/PI标记的细胞凋亡率，Westernblot方法检测cleavedcaspase-3、cleavedcaspase-9、PARP、cleavedPARP、Bcr/abl、p-AKT、p-mTOR蛋白表达。结果联合用药组对K562细胞的增殖抑制作用和诱导细胞凋亡率较单独用药组效果明显，差异均有统计学意义（均P＜0.01）。与单药组比较，联合用药组可以明显上调cleavedcaspase-3、cleavedcaspase-9、cleavedPARP蛋白表达，同时下调PARP、Bcr/abl、p-AKT、p-mTOR蛋白的表达，差异均有统计学意义（P＜0.01或0.05）。结论PD与IM联合用药在抑制细胞增殖、诱导凋亡、抑制Bcr/abl蛋白和PI3K/AKT/mTOR信号通路方面明显优于单独用药。 |
| 关键词: 梗皂甙 D 伊马替尼 K562 Bcr/abl 融合基因 PI3K//AKT/mTOR 信号途径 |
| DOI：10.12056/j.issn.1006-2785.2017.39.17.2017-622 |
| 分类号: |
| 基金项目:国家自然科学基金自助项目（81673755） |
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| Effect of platycodin D combined with imatinib on K562 cell in vitro |
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the First Affiliated Hospital of Zhejiang Chinese Medical University
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| Abstract: |
| Objective To investigate the effect and mechanism of Platycodin (PD) combined with imatinib (IM) on chronic myelogenous leukemia K562 cells in vitro. Methods Cultured K562 cells were treated with PD and imatinib alone or in combination. Cell proliferation was examined by CCK8 assay. Cell apoptosis were detected by Annexin V FITC/PI double staining. The change of mitochondrial trans-membrane potential was measured by JC-1 staining. The protein expression of cleaved caspase-3, cleaved caspase-9, PARP, cleaved PARP, Bcr/abl, p-AKT and p-mTOR were detected by Western blot. Results The inhibitory effects of PD combined with imatinib on proliferation and apoptosis of K562 cells were significantly higher than those of the control group or single drug groups (all P＜0.01). The expression of cleaved caspase-3, cleaved caspase-9 and cleaved PARP proteins was significantly up-regulated in the combination group, and the expression of PARP, Bcr/abl,
p-AKT and p-mTOR proteins was significantly down-regulated (P＜0.01 or 0.05). Conclusion Platycodin D combined with imatinib can significantly increase the inhibitory effect on cell proliferation and induce apoptosis of K562 cells compared with single drugs, which may be related to Bcr/abl protein and PI3K/AKT/mTOR signaling pathway. |
| Key words: PlatycodinD Imatinib K562 Bcr/abl fusion gene PI3K/AKT/mTOR signal pathway |
