摘要
目的观察表没食子儿茶素没食子酸酯(EGCG)对肝癌HepG2细胞Cyclin D1,Bcl-2表达的影响,探讨EGCG抗肿瘤的作用机制。方法采用MTT法观察EGCG对肝癌细胞HepG2增殖的影响,免疫细胞化学法、Western blot法分别检测EGCG作用后Cyclin D1,Bcl-2的表达。结果 EGCG呈浓度依赖性抑制肝癌HepG2细胞增殖(P<0.05),免疫细胞化学和Western blot的结果均显示EGCG作用后Cyclin D1和Bcl-2的表达下调。结论 EGCG可能通过下调Cyclin D1,Bcl-2的表达,抑制HepG2细胞增殖的同时诱导细胞凋亡,从而发挥抗肿瘤的作用。
【Objective】 To investigate the effects of epigallocatechin gallate(EGCG)on the HepG2 cells proliferation in vitro and to explore the probably mechanism of the anti-tumor activity of EGCG.【Methods】 The cell growth of human hepatocellular carcinoma cell line HepG2 was quantified by MTT assay.The expressions of the regulatory proteins of cell cycle such as Cyclin D1 and anti-apoptosis protein such as Bcl-2 in hepatocellular carcinoma cell line.HepG2 was detected by immunocytochemical staining and Western blot method.【Results】 When hepatocellular carcinoma cell line HepG2 was treated with EGCG after 48 h,the medicine inhibited the cells proliferation in a dose-dependent fashion.With the increase of concentration,the OD decreased.Compared with control group,the inhibitory effect on cell proliferation increased.Immunohistochemical method and Western blot method showed that the expressions of Cyclin D1 and Bcl-2 were decreased after EGCG treatment.【Conclusion】 EGCG may inhabit the proliferation of hepatocellular carcinoma cells HepG2 obviously.The underlying molecular mechanism is that EGCG inhabits the cell proliferation through down-regulating the expressions of the regulation proteins of cell cycle such as Cyclin D1 and the expressions of anti-apoptosis protein such as Bcl-2 to cause cell cycle arrest and induce apoptosis.So this medicine is promising as a kind of new medicines in hepatocellular carcinoma chemotherapy.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2012年第10期17-21,共5页
China Journal of Modern Medicine