摘要
目的:研究皂角刺总黄酮对肝癌HepG2细胞增殖、凋亡和侵袭的影响,探讨其抗肿瘤作用机制.方法:通过体外培养人肝癌HepG2细胞,用不同浓度的皂角刺总黄酮处理后,采用WST-1法检测皂角刺总黄酮对人肝癌细胞HepG2增殖的抑制作用,琼脂糖凝胶电泳检测DNA片段化,流式细胞仪AnnexinV/PI双染法检测细胞的凋亡率,划痕实验和Transwell小室检测皂角刺总黄酮对HepG2细胞侵袭、转移的影响.结果:不同浓度的皂角刺总黄酮作用于细胞48 h后,能显著抑制HepG2细胞的增殖,随着药物浓度的增加,抑制作用增强,IC50为(190.62±0.89)mg/L;流式AnnexinV/PI双染法检测显示,不同浓度的皂角刺总黄酮均可诱导HepG2细胞凋亡;不同浓度的皂角刺总黄酮处理组发现凋亡细胞所特有的DNA ladder条带;皂角刺总黄酮可降低HepG2细胞的黏附能力,使Tr-answell小室膜上的肝癌细胞明显减少,并且呈剂量依赖性.结论:皂角刺总黄酮能明显抑制肝癌HepG2细胞的增殖、侵袭能力和诱导其凋亡.
Objective: to investigate effects of flavone components from Spina gleditsiae on proliferation,apoptosis and invasion of HepG2 cell line,and explore its anti-tumor mechanism action.Methods: Human hepatocellular carcinoma HepG2 cells were cultured with medium,and were treated with different concentrations.The proliferation of HepG2 cells was observed by WST-1 assay.The apoptosis rate of HepG2 cells was observed by Flow Cytometry with Annexin-V/PI HepG2 staining,flavone components from Spina gleditsiae efficiently stimulated apoptosis in HepG2 cells as evidenced by DNA fragmentation,cells scratch assay and Transwell chamber assay were used to determine changes in invasion and migration of HepG2 cells after treatment.Results: The flavone components from Spina gleditsiae significantly inhibited the proliferation of HepG2 cells after 48 hours,and which in a dose-dependent manner,the IC50 value was(190.62±0.89) mg/L.After treatment of different concentration of flavone components from Spina gleditsiae,nuclear fragmentation was observed by HepG2 staining.The invasive and migrative ability of HepG2 cells could be obviously suppressed by the flavone components from Spina gleditsiae in a dose-dependent manner.Conclusion: Flavone components from Herb flavonoids can inhibit the proliferation of HepG2 cells and induce their apoptosis.
出处
《晓庄学院自然科学学报》
CAS
北大核心
2012年第1期77-81,共5页
Journal of Natural Science of Hunan Normal University
基金
2010年贵州省科学技术基金资助项目(黔科合J字[2010]2262号)
贵州省2011年社会发展科技攻关资助项目[黔科合SY字(2011)3020]
关键词
皂角刺总黄酮
HEPG2
增殖
凋亡
侵袭能力
flavone components from Spina gleditsiae
HepG2
proliferation
apoptosis
metastasi
