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PhaseoloidesideE诱导人肝癌HepG2细胞凋亡
引用本文:莫莎莎,舒广文,熊慧,赵寅,杨詹詹,梅之南. PhaseoloidesideE诱导人肝癌HepG2细胞凋亡[J]. 中国中药杂志, 2012, 37(10): 1494-1496
作者姓名:莫莎莎  舒广文  熊慧  赵寅  杨詹詹  梅之南
作者单位:中南民族大学药学院,湖北武汉,430074
基金项目:国家自然科学基金项目(81073150)
摘    要:
目的:以人肝癌HepG2细胞为研究对象,探讨phaseoloideside E(PE)的体外抗肿瘤活性。方法:采用MTT法,检测不同浓度的PE处理48 h后对HepG2细胞的细胞毒性效应;应用光学显微镜、荧光显微镜观察PE处理下的细胞形态学变化;用DNA琼脂糖凝胶电泳技术检测凋亡,并用免疫印迹法检测PE对凋亡相关蛋白Bax,Bcl-2表达水平的影响。结果:PE对HepG2细胞的生长有明显的细胞毒性效应;直接形态显微观察及Hoechst 33258荧光染色皆可见典型的凋亡细胞形态学特征;琼脂糖凝胶电泳结果显示给药组出现明显的DNA梯状凋亡带,而对照组没有出现梯状条带;免疫印迹结果显示PE可以增加Bax表达并减少Bcl-2表达。结论:PE能够诱导人肝癌HepG2细胞凋亡,并提示PE诱导的Bax,Bcl-2蛋白的表达水平变化可能与它的凋亡诱导效应紧密相关。

关 键 词:Phaseoloideside E  人肝癌HepG2细胞  凋亡
收稿时间:2011-11-04

Phaseoloideside E induces human hepatoma HepG2 cells apoptosis
MO Shash,SHU Guangwen,XIONG Hui,ZHAO Yin,YANG Zhanzhan and MEI Zhinan. Phaseoloideside E induces human hepatoma HepG2 cells apoptosis[J]. China Journal of Chinese Materia Medica, 2012, 37(10): 1494-1496
Authors:MO Shash  SHU Guangwen  XIONG Hui  ZHAO Yin  YANG Zhanzhan  MEI Zhinan
Affiliation:College of Pharmacy, South Central University for Nationalities, Wuhan 430074, China;College of Pharmacy, South Central University for Nationalities, Wuhan 430074, China;College of Pharmacy, South Central University for Nationalities, Wuhan 430074, China;College of Pharmacy, South Central University for Nationalities, Wuhan 430074, China;College of Pharmacy, South Central University for Nationalities, Wuhan 430074, China;College of Pharmacy, South Central University for Nationalities, Wuhan 430074, China
Abstract:
Objective: To study in vitro anti-tumor activity of phaseoloideside E (PE) with human hepatoma HepG2 cells as the objective. Method: MTT assay was adopted to detect the cytotoxic effect of PE of different concentrations on HepG2 cells after being processed for 48 h. Changes in morphology of PE-processed cells were observed under an optical microscope and fluorescence microscope. DNA agrose gel electrophoresis was used to detect the DNA ladder, an important characteristic of cell apoptosis. The expression levels of Bax and Bcl-2 were determined by western blot assay. Result: PE dramatically repressed the viability of HepG2 cells. Typical morphological changes of apoptosis had been detected by both direct microscopic observation and Hoechst 33258 staining. Typical DNA Ladder was also observed by agarose gel electrophoresis in the administration group, but it did not exist in the control group. Western blot showed that the expression of Bax was up-regulated and Bcl-2 was down-regulated. Conclusion: Above data demonstrates that PE can induce apoptosis in human hepatoma HepG2 cells, and indicate that PE-induced expression level changes of Bax and Bcl-2 may be related to the apoptosis-induction effect.
Keywords:phaseoloideside E  human hepatoma HepG2 cells  apoptosis
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