杨梅素作用于人肝癌HepG-2细胞凋亡信号转导途径的研究  

Studies on myricetin inducing human hepatoma HepG-2 cells apoptosis through signal transduction pathway

作　　者：张秀娟[1,2,3] 侯喆[1,2] 白雪莹[3] 季宇彬[1,2] 

机构地区：[1]哈尔滨商业大学生命科学与环境科学研究中心生物安全评价研究所,黑龙江哈尔滨150076 [2]哈尔滨商业大学国家教育部抗肿瘤天然药物教育部工程研究中心,黑龙江哈尔滨150076 [3]哈尔滨商业大学药学院,黑龙江哈尔滨150076

出　　处：《中国药理学通报》2014年第1期71-76,共6页Chinese Pharmacological Bulletin

基　　金：黑龙江省自然科学基金资助项目(No D201043)

摘　　要：目的研究杨梅素对肝癌HepG-2细胞凋亡的影响。方法 MTT法和SRB法分析杨梅素对肝癌HepG-2细胞增殖的影响,透射电镜和流式细胞仪分别观察杨梅素诱导HepG-2细胞凋亡作用,Western blot检测相关蛋白表达水平变化,分析杨梅素诱导HepG-2细胞凋亡机制。结果杨梅素以剂量依赖方式抑制肝癌HepG-2细胞的生长,IC50值为207.99μmol·L-1;杨梅素不同剂量组作用72 h后,HepG-2细胞表现出明显的凋亡特征,且HepG-2细胞G2/M期比例上升。HepG-2细胞中p-AKT,p-ERK和p-BAD蛋白随着剂量的增加表达水平均下降,AKT和ERK蛋白表达无明显改变。结论杨梅素可抑制HepG-2细胞增殖并诱导其凋亡,在一定浓度范围内呈剂量效应关系,并可将HepG-2细胞阻滞于G2/M期;通过下调p-AKT,p-ERK和p-BAD蛋白表达而起促凋亡作用。Aim To study the apoptosis of myricetin on human hepatoma HepG-2 cells. Methods The human hepatoma HepG-2 ceils were treated with myricetin and evaluated by MTT and SRB assay; the morphology of apoptosis was observed by transmission electron micros- copy（TEM） and flow cytometry （FCM）. The expres- sions of associated proteins were detected by Western blot to analyse the mechanism of apoptosis. Results Myricetin inhibited the growth of hepatoma cells in a dose-dependent manner, with IC50 values of 207.99 μmol·L^-1. After treatment with myricetin for 72h the characteristics of apoptosis of HepG-2 cells were ohserved. Myricetin increased the percentage of HepG-2 cells in G2/M phase. Western blot showed the expres- sions of p-AKT, p-ERK and p-BAD in HepG-2 cells decreased, but AKT and ERK were not obviously changed. Conclusion Myricetin could obviously in- hibit the proliferation and induce the apoptosis in HepG-2 cells in a dose-dependent manner, which may be related with the down-regulation of expressions of p- AKT, p-ERK, p-BAD.

关 键 词：杨梅素 HEPG-2细胞 增殖 凋亡 细胞周期 信号转 导途径 

分 类 号：R284.1[医药卫生—中药学] R329.24[医药卫生—中医学]