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油茶皂苷体外诱导人白血病Jurkat细胞凋亡及其可能机制
  • 期刊名称:肿瘤.2011, 31(12): 1072-1076.
  • 时间:0
  • 分类:R733.7[医药卫生—肿瘤;医药卫生—临床医学]
  • 作者机构:[1]大连大学生命科学与技术学院生物技术教研室,大连116622, [2]大连大学药物研究所中药室,大连116622, [3]美国堪萨斯州立大学人类营养系,堪萨斯州66502
  • 相关基金:国家自然科学基金资助项目(编号:30801509)
  • 相关项目:茶麸皂素抗肿瘤有效成分及作用机理研究
中文摘要:

目的:探讨油茶皂苷在体外诱导人白血病Jurkat细胞的凋亡及其可能机制。方法:将不同浓度的油茶皂苷作用于人白血病Jurkat细胞,应用细胞计数法检测其对细胞增殖的影响,FCM检测细胞周期分布和细胞凋亡率,蛋白质印迹法检测细胞caspase-3、多聚ADP-核糖聚合酶[poly(ADP-ribose)polymerase,PARP]、p-Bcl-2、Bcl-2、Bax和caspase-9蛋白的表达。结果:1~16μg/mL油茶皂苷可抑制Jurkat细胞的增殖,呈剂量依赖性。1~4μg/mL油茶皂苷作用Jurkat细胞24h后,G0/G1期和G2/M期细胞比率下降,S期细胞比率上升,细胞凋亡率随着油茶皂苷浓度的增加而上升;Jurkat细胞中,p-Bcl-2和Bcl-2蛋白的表达水平下调,caspase-3、PARP和caspase-9蛋白的表达水平上调,Bax蛋白的表达水平无明显变化。结论:油茶皂苷能抑制人白血病Jurkat细胞增殖和诱导其凋亡,其作用机制可能与细胞凋亡的线粒体途径有关。

英文摘要:

Objective: To investigate the apoptosis of human leukemiaJurkat cells induced by Youchasaponin in vitro and to explore its possible mechanism. Methods: The effects of Youchasaponin with different concentrations on the proliferation of Jurkat cells were detected by cell count assay. The cell cycle distribution and the apoptosis rate of Jurkat cells were determined by flow cytometry (FCM). The expression levels of caspase-3, poly (ADP-ribose) polymerase (PARP), p-Bcl-2, Bcl-2, Bax and caspase-9 proteins were analyzed by Western blotting. Results: The proliferation of Jurkat cells was significantly inhibited after treatment with Youchasaponin (1-16 μg/mL) in a dose-dependent manner. The percentage of Jurkat cells at G0/G1 phase and G2/M phase was decreased after treatment with Youchasaponin (1-4 μg/mL) for 24 h, while the percentage of Jurkat cells at S phase was increased. The apoptosis rate of Jurkat cells induced by Youchasaponin was increased in a dose-dependent manner. The expression levels of p-Bcl-2 and Bcl-2 proteins were down-regulated, and the expression levels of caspase-3, PARP and caspase-9 proteins were up-regulated, whereas the expression level of Bax protein had no change. Conclusion: Youchasaponin can inhibit the cell proliferation and induce the apoptosis of human leukemia cells. This effect may be related to the mitochondrial pathway of apoptosis.

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