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漆姑草醇提物对人白血病细胞株HL-60细胞凋亡相关蛋白表达的影响

Effects of Herba Saginae Japonicae alcohol extract on related to apoptosis protein of human leukemia cell line HL-60
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摘要 目的:研究漆姑草醇提物(HSJ)对人白血病细胞株HL-60细胞凋亡相关蛋白表达的影响,探讨其诱导凋亡的分子机制。方法:采用不同浓度的HSJ作用HL-60细胞后,Hoechst 33258荧光染色法检测细胞凋亡形态变化;Western blot法检测Caspase-3、Caspase-9、Bcl-2、Bax蛋白的表达。结果:HSJ作用后HL-60细胞出现浓染致密的颗粒状荧光及明显的核形态变化;与阴性对照组相比,凋亡相关蛋白Caspase-3、Caspase-9的表达水平增高,Bcl-2/Bax蛋白的比值降低,差异具有统计学意义(P<0.05)。结论:HSJ能诱导HL-60细胞凋亡,其作用可能与降低Bcl-2/Bax蛋白的比值,增加Caspase-9和Caspase-3蛋白表达水平有关。 Objective: To research the effect of Herba Saginae Japonicae(HSJ) alcohol extract on related to apoptosis protein of human leukemia cell line HL-60, and to explore mechanism underlying inductive apoptosis. Methods: HL-60 cells were treated by different dosages of HSJ. Hoechst 33258 fluorescent staining was used to detect apoptosis morphological changes. Western blot was used to detect the protein expression of Caspase-3, Caspase-9, Bcl-2 and Bax. Results: HL-60 cells processed by HSJ had been stained with condensed and dense fluorescence and showed obvious nuclear morphological changes. Compared with the control group, the expression level of apoptosis related to proteins including Caspase-3, Caspase-9 in the treatment group was increased, while the ratio of Bcl-2 to Bax was decreased. The difference was statistically significant(P〈0.05). Conclusion: HSJ could induce the apoptosis of HL-60 cells, which might be related to a decrease of the ratio of Bcl-2 to Bax and an increase of Caspase-9 and Caspase-3 protein expression.
出处 《中华中医药杂志》 CAS CSCD 北大核心 2016年第6期2380-2382,共3页 China Journal of Traditional Chinese Medicine and Pharmacy
基金 贵州省教育厅自然科学研究项目[No.黔教科(2010033号)]~~
关键词 漆姑草 HL-60细胞 细胞凋亡 CASPASE家族 BCL-2家族 Herba Saginae Japonicae HL-60 cells Apoptosis Caspase family Bcl-2 family
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  • 1WANG Guan-yu,ZHANG Jia-wei,LU Qing-hua,XU Rong-zhen,DONG Qing-hua.Berbamine induces apoptosis in human hepatoma cell line SMMC7721 by loss in mitochondrial transmembrane potential and caspase activation[J].Journal of Zhejiang University-Science B(Biomedicine & Biotechnology),2007,8(4):248-255. 被引量:15
  • 2Adams JM, Cory S. Life-or-death decisions by the Bcl-2 pro- tein family. Trends Biochem Sei 2001; 26:61-66.
  • 3Opferman JT, Korsmeyer SJ. Apoptosis in the development and maintenance of the immune system. Nat Immunol 2003; 4:410-415.
  • 4Antignani A, Youle RJ. How do Bax and Bak lead to permea- bilization of the outer mitochondrial membrane? Curr Opin Cell Bio12006; 18:685-689.
  • 5Green DR, Kroemer G. The pathophysiology of mitochon- drial cell death. Science 2004; 305:626-629.
  • 6Kim H, Rafiuddin-Shah M, Tu HC, et al. Hierarchical regula- tion of mitochondrion-dependent apoptosis by BCL-2 sub- families. Nat Cell Bio12006: 8:1348-1358.
  • 7Willis SN, Fletcher JI, Kaufmann T, et al. Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak. Science 2007; 315:856-859.
  • 8Sattler M, Liang H, Nettesheim D, et al. Structure of Bcl- xL-Bak peptide complex: recognition between regulators of apoptosis. Science 1997; 275:983-986.
  • 9Liu X, Dai S, Zhu Y, Marrack P, Kappler JW. The structure of a Bcl-xL/Bim fragment complex: implications for Bim func- tion. Immunity 2003; 19:341-352.
  • 10Petros AM, Nettesheim DG, Wang Y, et al. Rationale for Bcl- xL/Bad peptide complex formation from structure, mutagen- esis, and biophysical studies. Protein Sci 2000; 9:2528-2534.

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