人参皂苷CK诱导人肝癌SMMC-7721细胞凋亡的内质网应激作用机制  

Ginsenoside CK induces apoptosis in human liver cancer cells by endoplasmic reticulum stress pathway

作　　者：魏群[1] 张璇[2] 张学武[2] WEI Qun;ZHANG Xuan;ZHANG Xue-wu(Henan University of Chinese Medicine,Zhengzhou,Henan,450046,China;College of Medicine,Yanbian University,Yanji,Jilin,133000,China)

机构地区：[1]河南中医药大学,河南郑州450046 [2]延边大学医学院,吉林延吉133000

出　　处：《时珍国医国药》2018年第12期2896-2899,共4页Lishizhen Medicine and Materia Medica Research

基　　金：国家自然科学基金(81760728)

摘　　要：目的探讨人参皂苷CK对人肝癌SMMC-7721细胞凋亡作用及其作用机制。方法通过体外培养SMMC-7721细胞,分为空白对照组、阳性对照组(5-Fu)和人参皂苷CK药物组,采用MTT法测定不同浓度人参皂苷CK (20,40,60μmol/L)对人肝癌SMMC-7721细胞增殖的影响;通过Hoechst染色观察人参皂苷CK诱导人肝癌SMMC-7721细胞凋亡的形态学变化;利用流式细胞术检测细胞凋亡比例; Western Blot检测凋亡相关蛋白Cleaved-caspase 3和内质网应激相关蛋白(GRP78、p-JNK、Cleaved-caspase 4和CHOP)的表达情况。结果人参皂苷CK可显著地抑制人肝癌SMMC-7721细胞的增殖,且随着药物浓度的升高,抑制作用逐渐增加。同时,随着药物浓度的增加,典型凋亡形态特征的细胞逐渐增多,凋亡蛋白Cleaved-caspase 3及内质网应激相关蛋白GRP78、p-JNK、Cleaved-caspase 4、CHOP的表达均逐渐升高。结论人参皂苷CK可以抑制人肝癌SMMC-7721细胞生长并诱导细胞凋亡,其作用机制可能与激活内质网应激有关。Objective To investigate the effect of ginsenoside CK on apoptosis of human liver cancer cells SMMC-7721 and the mechanism. Methods SMMC-7721 cells were treated with CK( 20,40,60 μmol/L),and cell vaibility was measured by MTT assay;Morphological changes of SMMC-7721 cells were observed by Hoechst staining;Flow cytometry was used to detected the CK-induced apoptosis. The protein expression of Cleaved-caspase 3,GRP78,p-JNK,Cleaved-caspase 4 and CHOP were analyzed by western blotting. Results Ginsenoside CK inhibited the vaibility of SMMC-7721 cells in does-dependent manner.Comparing with control group,CK groups altered cell morphology and increased apoptosis-related blue/white cells,and the expression of Cleaved-caspase3,GRP78,p-JNK,Cleaved-caspase 4 and CHOP were increased obviously. Conclusion Ginsenoside CK induced apoptosis of SMMC-7721 cells and the main mechanism are related to endoplasmic reticulum stress pathway.

关 键 词：人参皂苷CK SMMC-7721细胞 细胞凋亡 内质网应激 

分 类 号：R285.5[医药卫生—中药学]