紫草素通过PI3K/Akt通路促进人乳腺癌MCF-7细胞自噬  

Shikonin promotes autophagy of MCF-7 human breast cancer cells through PI3K/Akt pathway

作　　者：陈菊英[1] 刘朝纯[1] 曾智[1] 黄文东[1] 杨永飞[1] 朱邦豪[1] 

机构地区：[1]中山大学中山医学院药理学教研室,广东广州510080

出　　处：《中国药理学通报》2013年第2期194-198,共5页Chinese Pharmacological Bulletin

基　　金：粤港关键领域重点突破项目(No 2007A032702001)

摘　　要：目的研究紫草素(Shikonin)对人乳腺癌MCF-7细胞自噬的影响及其作用机制。方法 CCK-8法检测紫草素处理人乳腺癌MCF-7细胞24、48 h细胞的存活率,Western blot方法检测紫草素处理24 h和48 h时LC3、p62、PI3K、Akt、p-PI3K、p-Akt蛋白水平。结果 1μmol.L-1紫草素处理细胞48 h以及2.5、5μmol.L-1紫草素处理MCF-7细胞24 h和48 h时,MCF-7细胞的活力受到明显抑制,LC3-Ⅱ/LC3-Ⅰ值增加,p62表达减少,总PI3K、Akt、p-PI3K、p-Akt均减少。结论紫草素促进乳腺癌MCF-7细胞自噬,其作用机制可能与PI3K/Akt通路受到抑制有关。Aim To explore the effect of shikonin on the autophagy of MCF-7 human breast cancer cells and its mechanism.Methods The cell viabilities were examined by CCK-8 assay.And the expressions of LC3,p62,PI3K,Akt,p-PI3K,p-Akt were tested by western blot assay.Results The cell viabilities of MCF-7 cells were significantly inhibited,the values of LC3-Ⅱ/LC3-Ⅰ were elevated,and the protein levels of p62,PI3K,Akt,p-PI3K,p-Akt were all decreased after treated with 1 μmol·L^-1 shikonin 48 h and 2.5,5 μmol·L-1 shikonin 24 h,48 h.Conclusions Shikonin can promote the autophagy of MCF-7 cells,and the possible mechanism is related to the PI3K/Akt signaling pathway.

关 键 词：紫草素 MCF-7细胞 自噬 LC3 P62 PI3K Akt p-PI3K P-AKT 

分 类 号：R284.1[医药卫生—中药学] R329.25[医药卫生—中医学]