油茶皂苷通过内质网应激途径诱导人肝癌细胞HepG2凋亡的研究  

Study on Youchasaponin-induced apoptosis of HepG2 cells through the endoplasmic reticulum stress

作　　者：马丽媛[1,2] 李林[1,2] 江玉 史丽颖[1,2] 冯宝民[1,2] 王永奇[1,2] 唐玲[1,2] 

机构地区：[1]大连大学生命科学与技术学院,usa66502 [2]大连大学药物研究所,辽宁大连116622 [3]Kansas State University,Human Nutrition,kansasusa66502

出　　处：《中国药理学通报》2011年第11期1523-1527,共5页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No30801509)

摘　　要：目的探讨油茶皂苷诱导人肝癌细胞HepG2凋亡的作用及其作用机制。方法采用MTT法考察了油茶皂苷对肿瘤细胞增殖的影响;用Western blot方法分析油茶皂苷对caspase-3、PARP、Bip、ATF6、IRE1、Perk、eIF2a和eEF2蛋白质表达的影响。结果油茶皂苷(10～30 mg.L-1)明显抑制HepG2细胞的增殖。同时可激活Caspase信号通路,诱发PARP底物的断裂;进一步上调IRE1表达量及活化Perk、eIF2a和eEF2蛋白。结论油茶皂苷通过内质网应激途径诱导人肝癌细胞HepG2发生凋亡。Aim To investigate the inducing effect of Youchasaponin on the apoptosis of human hepatoma carcinoma cell HepG2 in vitro.Methods Effects of Youchasaponin on the proliferation of HepG2 cells were detected by MTT assay;effects on the expression of caspase-3,PARP,Bip,ATF6,IRE1,Perk,eIF2a and eEF2 were analyzed by Western blot.Results The proliferation of HepG2 cells was significantly inhibited after treatment with Youchasaponin（10~30 mg·L-1）,and meanwhile it activated caspase pathway,induced the fracturing of PARP substrate and furtherly increased the expression of IRE1,and activate Perk,eIF2a,and eEF2.Conclusion Youchasaponin induces the apoptosis of HepG2 through endoplasmic reticulum stress pathway.

关 键 词：油茶皂苷 抗肿瘤 人肝癌细胞株(HepG2) 内质网应激 人免疫球蛋白重链结合蛋白(Bip) RNA激活蛋白激酶的内质网类似激酶(Perk) 

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