杨梅素对HepG2细胞凋亡的影响  

The effect of myricetin on HepG2 apoptosis

作　　者：郭海清[1] 任锋[2] 陈亚利[1] 张向颖[2] 段钟平[3] 孙华[4] 张晶[1] 

机构地区：[1]首都医科大学附属北京佑安医院中毒性肝病科,100069 [2]首都医科大学附属北京佑安医院北京市肝病研究所,100069 [3]首都医科大学附属北京佑安医院人工肝中心,100069 [4]中国医学科学院药物研究所药理室

出　　处：《北京医学》2014年第9期748-751,F0002,共5页Beijing Medical Journal

基　　金：北京市卫生系统高层次卫生技术人才培养计划(2013-3-075;2011-3-082);北京市中医药科技发展基金(JJ2011-06)

摘　　要：目的探讨杨梅素对人肝癌细胞系HepG2凋亡的影响及其机制。方法以不同浓度的杨梅素孵育HepG2细胞,在不同时间分别采用倒置显微镜观察细胞形态学变化;采用噻唑蓝(MTT)法检测细胞存活率;采用乳酸脱氢酶(LDH)活力定量测定试剂盒测定细胞上清液LDH活性;采用流式细胞术检测细胞凋亡率;采用蛋白质印迹法检测细胞凋亡途径关键蛋白的表达。结果杨梅素对HepG2细胞的凋亡诱导作用呈现剂量和时间依赖性。杨梅素作用于HepG2细胞,随杨梅素浓度增加,细胞凋亡率增加。与正常对照组相比,100μmol/L杨梅素作用于HepG2细胞24 h后,细胞存活率明显降低[(100.02±5.97)%vs.(71.60±3.75)%,P=0.006];早、晚期细胞凋亡率明显升高[(10.19±2.61)%vs.(2.52±2.05)%,P=0.003;(11.71±3.34)%vs.(3.69±1.13)%,P=0.004],差异均有统计学意义。随杨梅素浓度增加,线粒体途径的促凋亡因子BAX蛋白表达量增加,而抗凋亡因子BCL-2蛋白表达量降低。结论杨梅素能够诱导HepG2细胞凋亡,可能具有潜在的抗肝癌活性;线粒体途径在此过程中起重要作用。Objective To study the effect of myricetin on HepG2 apoptosis. Methods HepG2 cell was incubated with different concentrations of myricetin. Cell viability was measured by MTT method. Apoptosis was measured by flow cytometry. The expressions of the key protein of apoptosis were detected by western blot. Results The reduction of cell viability was more significant with the increase of myricetin concentration. In the 100μmol/L myricetin for 24 h group,the cell viability was lower than the control group[（71.6±3.75）% vs.（100.02±5.97）%,P = 0.006], the early and late apoptosis rate were higher than the control group[（10.19±2.61）% vs.（2.52±2.05）%,P = 0.003;（11.71±3.34）% vs.（3.69±1.13）%,P = 0.004]. The expression of pro-apoptotic factor BAX protein was increased, while the anti-apoptotic factor BCL-2 protein expression was reduced. Conclusion Myricetin could induce apoptosis of HepG2 cell through mitochondrial pathway,indicating that myricetin might inhibit hepatocellular carcinoma progression.

关 键 词：杨梅素 HEPG2细胞 凋亡 线粒体途径 

分 类 号：R735.7[医药卫生—肿瘤]