摘要
目的研究干扰素(IFN)和小剂量阿糖胞苷(Ara-C)联合应用对K562细胞的诱导凋亡作用,并探讨其机制。方法以IFN-α2b和小剂量Ara-C单独和联合作用后,MTT法检测K562细胞的生长抑制率,流式细胞仪检测细胞凋亡水平,RT-PCR检测野生型p53基因的表达,免疫细胞化学法检测野生型P53蛋白的表达。结果IFN-α2b和小剂量Ara-C联合作用可以有效抑制K562细胞的增殖,联合作用后K562细胞的抑制率可达42.85%,与对照组及单用IFN-α2b和单用Ara-C相比,差异均有显著性意义(均P<0.05)。IFN-α2b和小剂量Ara-C联合作用72 h后,可以使K562细胞凋亡率提高到39.03%,与对照组及单用IFN-α2b和单用Ara-C相比,差异均有显著性意义(均P<0.05)。两药联合作用可以促进野生型p53基因mRNA和蛋白的表达上调。结论联合使用IFN和小剂量Ara-C可以协同诱导K562白血病细胞的凋亡,促进野生型p53基因和蛋白表达上调可能是其机制之一。
Objective To investigate the mechanisms of apoptosis of K562 induced by interferon （IFN） combined with low-dose cytarabine-C （Ara-C）. Methods K562 cells were treated with IFN-α 2b and low-dose Ara-C. The growth inhibitory rate was detected by MTT, apoptosis by flow cytometry, the expression of wide type p53 mRNA by RT-PCR, and the expression of wide type P53 protein by immunocytochemistry. Results After treated with IFN-α 2b and low-dose Ara-C, the inhibitory rate of K562 cells, compared with that in the control, was increased to 42.85 %, and the apoptotic rate of K562 cells was increased from 3.88 % to 39.03 %. Apoptosis of K562 was accompanied by the expression of wide type p53 mRNA and protein. The transcription of the p53 gene was induced by IFN-α 2b and low-dose Ara-C, accompanied by an increase in P53 protein level. Conclusion IFN combined with low-dose Ara-C can induce apoptosis of K562 cells. Wide type p53 is contributed to the apoptosis of the cells induced by IFN combined with low-dose Ara-C.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2006年第3期336-338,342,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
湖北省卫生厅重点科研基金资助项目(No.JX2A10)
