期刊文献+

复方肝癌宁含药血清诱导肝癌HepG_2细胞凋亡的实验研究 被引量:6

Apoptosis of human hepatocellular carcinoma cell line HepG_2 induced by composite Gan'aining medicated serum in vitro
下载PDF
导出
摘要 目的:观察复方肝癌宁含药血清对肝癌HepG2 细胞凋亡的诱导作用.方法:运用中药血清药理学方法,选择不同浓度的含药血清与人肝癌HepG2细胞共同孵育观察,并与阳性血清组、无药血清组作对照.结果:复方肝癌宁含药血清可显著抑制HepG2 细胞的增长;TUNEL法检测HepG2细胞在显微镜下呈现典型的凋亡形态学改变,可见“凋亡小体”,高、中、低剂量含药血清组凋亡率分别为:14.50%,13.61%和10.19%,与无药血清组比较P<0.01;流式细胞仪检测可见亚G1峰, 凋亡呈含药血清浓度依赖性特点,高、中、低剂量含药血清组凋亡率分别为15.1%,12.0%, 5.5%.与无药血清组比较P<0.01或P<0.05 结论:复方肝癌宁可通过诱导肿瘤细胞凋亡, 发挥临床抗肝肿瘤、抗转移的作用. AIM: To investigate the efficacy of compsite Gan'aining (CGN) in inducing the apoptosis of human hepatocellular carcinoma (HCC) cell line HepG2 in vitro. METHODS: Human HCC HepG2 cells were cocultured with non-medicated serum, 5-FU medicated serum, and different concentrations of CGN medicated serum, respectively. The apoptosis of HepG2 cells was detected by TUNEL and flow cytometry (FCM), respectively. RESULTS: CGN medicated Serum at different concentrations inhibited the growth of HepG2 cells in vitro. After treatment with CGN, typical features of apoptosis such as apoptotic body were observed under light microscope. High-, moderate- and low-dose CGN medicated serum induced apoptotic rates (by TUNEL) of 14.5% + 1.81%, 13.61% ± 1.78% and 10.19% ± 1.77%, respectively, which were significantly higher than that induced by non-medicated serum (0.74% ± 0.12%)(all P 〈 0.01). The sub-G1 peaks were observed by FCM in CGN treated cells and the apoptosis rates of the cells treated with high-, moderate- and low-dose CGN medicated serum were 15.1%, 12%, and 5.5%, respectively, which were markedly higher than that of the cells treated with non-medicated serum (1.0%)(P 〈 0.01 or P 〈 0.05). CONCLUSION: CGN can induce the apoptosis of human HCC cells in vitro in a dose-dependent manner.
出处 《世界华人消化杂志》 CAS 北大核心 2006年第5期522-525,共4页 World Chinese Journal of Digestology
基金 广东省科技厅科技计划资助项目 No.2005B33001032~~
关键词 复方肝癌宁 HEPG2 流式细胞术 细胞凋亡 血清药理学 Composite Gan'aining Apoptosis HepG2 cell line Serum pharmacology
  • 相关文献

参考文献14

二级参考文献124

共引文献213

同被引文献64

引证文献6

二级引证文献33

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部