枸橼醛在急性早幼粒细胞白血病细胞系K562中的作用

赵艳秋*

doi:10.16098/j.issn.0529-1356.2017.03.010

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解剖学报 ›› 2017, Vol. 48 ›› Issue (3) : 310-315. DOI: 10.16098/j.issn.0529-1356.2017.03.010

肿瘤生物学

枸橼醛在急性早幼粒细胞白血病细胞系K562中的作用

赵艳秋*

作者信息 +

Effect of citral on k562 cell line in vitro

ZHAO Yan-qiu*

Author information +

文章历史 +

摘要

目的探讨枸橼醛（citral）在急性早幼粒细胞白血病细胞系K562中的作用。方法 Citral作用于体外培养K562细胞系，分别用Wright-Giemsa染色观察细胞凋亡形态；MTT法计算细胞增殖能力；DNA电泳分析DNA碎片；Annexin V-FITC/PI分析细胞凋亡变化；RT-PCR法检测凋亡通路蛋白Bcl、Bax的表达水平变化；流式细胞术分析线粒体膜电位、Caspase-3和核因子（NF)-κB水平变化。结果 Citral以时间和剂量依赖性方式诱导K562细胞凋亡，citral能够诱导线粒体膜电位减少。证实citral诱发细胞凋亡是依赖线粒体途径。结论 Citral对白血病有潜在的治疗效果，有一定的临床应用前景。

Abstract

Objective To investigate the effect of citral on the acute early young granulocyte leukemia cell line K562. Methods The apoptosis morphology was observed. Diffusion test, DNA electrophoresis, membrane proteins V-FITC/PI staining and Caspase activation in K562 cells were performed to evaluate the effect of citral on the role of K562. Results Citral induced the apoptosis of K562 cells in a time and dose dependent manner. Citral also induced the decreasing of mitochondrial membrane potential(MMP). Conclusion Citral has a potential effect in leukemia treatment and clinical application.

导出引用

赵艳秋. 枸橼醛在急性早幼粒细胞白血病细胞系K562中的作用[J]. 解剖学报. 2017, 48(3): 310-315 https://doi.org/10.16098/j.issn.0529-1356.2017.03.010

ZHAO Yan-qiu. Effect of citral on k562 cell line in vitro[J]. Acta Anatomica Sinica. 2017, 48(3): 310-315 https://doi.org/10.16098/j.issn.0529-1356.2017.03.010

参考文献

［1］Zhang W, Zhang RW, Zhu WH,et al. Mechanism of apoptosis in HeLa cells induced by quinine［J］.Acta Anatomica Sinica, 2015 Vol.46(5):641-645.(in Chinese)

张巍，张若文，朱文赫，等. 胡桃醌诱导HeLa细胞凋亡的机制［J］.解剖学报，2015,46(5):641-645.

［2］Adams JM. Ways of dying: multiple pathways to apoptosis［J］. Genes Dev, 2013, 17(20):2481-2495.

［3］Wang CY, Mayo MW, Korneluk RG, et al. NF-kappaB anti apoptosis: induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to suppress caspase-8 activation［J］. Science, 2014, 281(5383): 1680-1683.

［4］Micheau O, Lens S, Gaide O, et al. NF-{kappa}B signals induce the expression of c-FLIP［J］. Mol Cell Biol, 2012, 21(6): 5299-5305.

［5］Gilmore T, Koedood M, Piffat K, et al. Rel/NF-κB/IκB proteins and cancer［J］. Oncogene, 2014, 13(7):1367-1378.

［6］Rayet B, Gelinas C. Aberrant Rel/NF-κB genes and activity in human cancer［J］. Oncogene, 2015, 18(49):6938-6947.

［7］McKeithan TW, Takimoto GS, Ohno H. Bcl-3 rearrangements and t(14;19) in chronic lymphocytic leukemia and other B-cell malignancies: a molecular and cytogenetic study［J］. Genes Chromosomes Cancer, 2013, 20(1):64-72.

［8］Chaouki W, Leger DY, Liagre B, Citral inhibits cell proliferation and induces apoptosis and cell cycle arrest in MCF-7 cells［J］. Fundam Clin Pharmacol, 2014, 23(5):549-556.

［9］Dudai N, Weinstein Y, Krup M, et al. Citral is a new inducer of caspase-3 in tumor cell lines［J］. Planta Med, 2015, 71(5):484-488.

［10］Mendon?a Ade L, da Silva CE, de Mesquita FL, et al. Antimicrobial activities of components of the glandular secretions of leaf cutting ants of the genus Atta［J］. Antonie Van Leeuwenhoek, 2012, 95(4):295-303.

［11］Karin M, Greten FR. NF-κB: linking inflammation and immunity to cancer development and progression［J］. Nature Rev Immunol, 2015, 5(10): 749-759.

［12］Vallabhapurapu S, Karin M. Regulation and function of NF-kappaB transcription factors in the immune system［J］. Annu Rev Immunol, 2009, 27: 693-733.

［13］Zhu BS, Xing ChG, Lin F, et al. Blocking NF-κB nuclear translocation leads to p53-related autophagy activation and cell apoptosis［J］. World J Gastroenterol, 2011，17(4): 478-487.