中文摘要：

目的：研究飞燕草素对HER-2^＋乳腺癌细胞MDA-MB-453自噬的诱导作用及其分子机制。方法：以不同浓度飞燕草素处理MDA-MB-453细胞,CCK-8检测细胞增殖情况;TdT介导的脱氧尿嘧啶缺口末端标记（TdT-mediated dUTP nick end labeling,TUNEL）和Western印迹检测细胞凋亡和与凋亡相关蛋白的表达;荧光斑点、免疫荧光和Western印迹检测自噬的诱导情况和诱导机制。结果：飞燕草素抑制MDA-MB-453细胞增殖,增加TUNEL阳性细胞数,下调caspase-3和caspase-9蛋白活性,上调裂解的caspase-3和裂解的caspase-9蛋白活性。飞燕草素增加GFP-LC3荧光斑点数、LC3免疫荧光斑点数、LC3-Ⅱ和ATG5蛋白表达。飞燕草素下调mTOR通路蛋白AKT,mTOR,eIF4E和p70s6k蛋白活性。结论：飞燕草素诱导HER-2^＋乳腺癌细胞MDA-MB-453凋亡的同时通过抑制AKT/mTOR通路诱导细胞自噬。

英文摘要：

Objective： To explore the effect of delphinidin on breast cancer and the underlying mechanisms. Methods： Human epidermal growth factor receptor-2（HER-2） positive breast cancer cells MDAMB-453 were treated by delphinidin. Proliferation of MDA-MB-453 cells was detected by CCK-8 after 48 h. Td T-mediated d UTP nick end labeling（TUNEL） assay and Western blot were used to explore apoptotic status for MDA-MB-453 cells. Fluorescence dot assay, immunofluorescence, and Western blot were used to identify autophagy in breast cancer cells. Results： Delphinidin suppressed proliferation of MDA-MB-453 cells. Delphinidin increased the number of TUNEL positive cells. Delphinidin downregulated the expression of caspase-3 and caspase-9, while upregulated the expression of cleaved caspase-3 and cleaved caspase-9 in a dose-dependent manner. Delphinidin enhanced the number of GFP-LC3 punctate dots, LC3 immunofluorescence dots and the expression of LC3-Ⅱ and ATG5. Delphinidin inhibited the expression of proteins in m TOR signaling pathway, including AKT, mTOR, eIF4E and p70s6 k. Conclusion： Delphinidin induced apoptosis and autophagy by inhibition of AKT/mTOR pathway in HER positive breast cancer cells.