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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 study the effect of total flavonoids from Gleditsia sinensis on the proliferation, apoptosis and invasion of HepG2 hepatocellular carcinoma cells and to explore the mechanism of its anti-tumor effect.Methods: HepG2 cells were cultured in vitro, treated with different concentrations of total flavonoids, WST-1 method was used to detect the inhibitory effect of total flavonoids of Grifola frondosa on the proliferation of human hepatoma HepG2 cells. DNA fragmentation was detected by agarose gel electrophoresis. Cell apoptosis rate and scratch were detected by flow cytometry Annexin V / PI double staining Experiments and Transwell chambers were used to detect the effect of total flavonoids of Gleditsia sinensis on the invasion and metastasis of HepG2 cells.Results: The total flavonoids of Gleditsia sinensis could significantly inhibit the proliferation of HepG2 cells after treated with total flavonoids for 48 h, with the increase of drug concentration (190.62 ± 0.89) mg / L. The results of flow cytometry with Annexin V / PI double staining showed that different concentrations of total flavonoids of Gleditsia sinensis can induce apoptosis of HepG2 cells. Different concentrations of Gleditsia sinensis Flavone treatment group found DNA ladder band characteristic apoptosis cells; saponin thorn total flavonoids can reduce HepG2 cell adhesion capacity, so that Tr-answell small cell membrane on the liver cancer cells decreased significantly and in a dose-dependent manner.Conclusion: soap Angle thorn total Ketones could significantly inhibit the proliferation of HepG2 cells and invasion, and induces apoptosis.