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作 者:钟志宏[1] 陈文贵[2] 柳永和[2] 李启星[1] 邱月[1]
机构地区:[1]湖南师范大学医学院,长沙410006 [2]湘雅医学院情报与信息技术学院,长沙410078
出 处:《中南大学学报(医学版)》2007年第1期99-103,共5页Journal of Central South University :Medical Science
基 金:湖南师范大学青年基金~~
摘 要:目的:研究丹参酮ⅡA对人肝癌细胞HepG2的生长抑制作用和凋亡诱导作用。方法:以0μg/mL丹参酮ⅡA作阴性对照,MTT法检测0.5~10.0μg/mL丹参酮ⅡA作用人肝癌细胞HepG224,48,72h的生长抑制率;HT33258荧光染色、琼脂糖凝胶电泳、流式细胞仪检测不同浓度丹参酮ⅡA作用HepG2细胞72h后的细胞凋亡。结果:0.5~10.0μg/mL丹参酮ⅡA均能抑制人肝癌细胞HepG2生长,并有明显的时间和剂量依赖性;在24,48,72h的半数抑制浓度分别为14.7,7.4,3.9μg/mL;经丹参酮ⅡA作用后,荧光染色可以观察到典型的凋亡细胞形态特征;琼脂糖凝胶电泳结果显示除1.0μg/mL组外均可见明显的凋亡细胞形成的梯状条带;流式细胞仪检测不同浓度丹参酮ⅡA作用72h后的细胞凋亡率分别为20.32%±2.16%,28.01%±2.35%,33.87%±3.43%,46.73%±4.08%和57.85%±3.74%,与对照组比较差异均有统计学意义(P<0.05)。结论:丹参酮ⅡA在体外能明显抑制人肝癌细胞HepG2生长,抑制其生长的机制可能是诱导细胞凋亡。Objective To determine the effect of tanshinone Ⅱ A on the growth and apoptosis in human hepatoma cell line HepG2. Methods The human hepatoma cell line HepG2 was treated with tanshinone Ⅱ A at various concentrations for 72 h. The inhibition of proliferation was measured by MTT assay and apoptosis-related alterations in morphology measured by cytochemical staining (HT33258). DNA fragmentation was evaluated by agarose gel eleetrophoresis. Apoptotic rate and cell arrest were quantified by flow cytometry ( FCM ). Results Tanshinone Ⅱ A inhibited the growth of HepG2 in a time- and dose- dependent manner. The semi-inhibitory concentration (IC50) value after the treatment with tanshinone II A on HepG2 for 24,48, and 72 h were 14.7,7.4, and 3.9 μg/ mL, respectively. After the treatment with 0.5 - 10 μg/mL tanshinone II A for 72 h, the formation of apoptotic bodies was observed. DNA ladder was shown in agarose gel electrophoresis, in additionn to the cells treated by 1.0 μg/mL tanshinone Ⅱ A . The apoptotic rates at 0.5, 1.0,2.0, 5.0, and 10. 0 μg/mL for 72 h were 20. 32% ±2. 16%,28. 0%±2. 35%,33. 87% ± 3.43%,46.73% :t=4.08% and 57. 85% ± 3.74%, respectively, which were all significantly higher than those of the control group ( P 〈 0.05 ). Conclusion Tanshinone Ⅱ A can inhibit the proliferation of human hepatoma cell line HepG2 in a time- and dose- dependent manner, and the mechanism of growth inhibition of human hepatoma cells may be related to the induction of apoptosis.
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