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作 者:姜爽[1] 任艳平 魏琳 孙晓琦 武天琦 郭焱[1] 刘智[1] 宋伍 JIANG Shuang;REN Yan-ping;WEI Lin;SUN Xiao-qi;WU Tian-qi;GUO Yan;LIU Zhi;SONG Wu(Changchun University of Chinese Medicine,Changchun 130117,China;Xiuzheng Pharmaceutical Group Changchun High-tech Pharmaceutical Co.,Ltd.,Changchun 130021,China)
机构地区:[1]长春中医药大学,吉林长春130117 [2]修正药业集团长春高新制药有限公司,吉林长春130021
出 处:《中成药》2018年第9期1925-1929,共5页Chinese Traditional Patent Medicine
基 金:吉林省教育厅"十三五"科学技术研究项目(吉教科合字[2016]第27号)
摘 要:目的探讨人参皂苷CK对人乳腺癌MCF-7细胞增殖、凋亡、上皮间质转化、PI3K/Akt信号通路的影响。方法 MCF-7细胞经不同浓度的人参皂苷CK处理后,MTT法检测细胞增殖,流式细胞术检测细胞凋亡,real-time q PCR法检测E-钙黏蛋白、N-钙黏蛋白、波形蛋白mRNA表达,Western blot法检测p-PI3K、p-Akt蛋白表达。结果与对照组比较,10μmol/L人参皂苷CK处理72 h,20、40、80μmol/L人参皂苷CK处理24、48、72 h后,对细胞增殖的抑制率显著增加(P<0.05);20、40、80μmol/L人参皂苷CK处理48 h后,细胞凋亡率和E-钙黏蛋白mRNA表达显著增加(P<0.05);20、40、80μmol/L人参皂苷CK处理48 h后,N-钙黏蛋白、波形蛋白mRNA表达,以及p-PI3K、p-Akt蛋白表达显著降低(P<0.05)。结论人参皂苷CK可抑制MCF-7细胞增殖、上皮间质转化,并诱导细胞凋亡,这可能与抑制PI3K/Akt信号通路相关。AIM To explore the effects of ginsenoside CK on the proliferation,apoptosis,epithelial-mesenchymal transition and PI3K/Akt signaling pathway of human breast cancer MCF-7 cells.METHODS The breast cancer MCF-7 cells treated with different concentrations of ginsenoside CK had their cell proliferation,cell apoptosis,mRNA expressions of E-cadherin,N-cadherin and vimentin,protein expressions of p-PI3K and p-Akt detected by MTT,flow cytometry,real-time qPCR and Western blot,respectively.RESULTS Compared with the control group,groups treated with 10μmol/L ginsenoside CK for 72 h,and 20μmol/L,40μmol/L,80μmol/L ginsenoside CK for 24,48,72 h,respectively,shared significantly increased inhibition rates of cell proliferation(P<0.05);groups treated with 20,40,80μmol/L ginsenoside CK for 48 h shared obviously increased cell apoptosis rate and E-cadherin mRNA expression(P<0.05);groups treated with 20,40,80μmol/L ginsenoside CK for 48 h were found with markedly decreased N-cadherin,vimentin mRNA expressions,and p-PI3K,p-Akt protein expressions(P<0.05).CONCLUSION Ginsenoside CK’s inhibition on the proliferation and epithelial-mesenchymal transition of MCF-7 cells,and induction of cell apoptosis may be related to the inhibition of PI3K/Akt signaling pathway.
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