中文摘要：

目的：观察D-鼠李糖β常春藤甙（简称D药）对乳腺癌细胞的杀伤作用,通过研究其对PI3K/AKT信号通路的影响,探索其抗肿瘤机制。方法：不同浓度D药作用于乳腺癌细胞株MCF-7、MDA-MB-231 48 h后,流式细胞仪Annexin V-FITC/PI双染法检测细胞凋亡率,Western blot法检测D药作用MCF-7、MDA-MB-231后PI3K/AKT信号通路相关分子的蛋白表达。结果：20、30、40μg/ml D药作用细胞48 h后可以诱导细胞凋亡,凋亡率随浓度升高而增加。20μg/ml D药作用细胞48 h后,pPI3K、p-AKT蛋白表达减少,而总PI3K、总AKT蛋白的表达量无明显变化。PI3K抑制剂LY294002通过抑制细胞p-AKT的表达,从而增加D药引起的细胞凋亡。结论：D药可以通过抑制PI3K的磷酸化,进而影响磷酸化AKT的表达,最终诱导乳腺癌细胞凋亡。

英文摘要：

Objective：To study the effect of D-Rhamnose β hederin on the apoptosis of breast cancer cells and its effect on PI3K/ AKT signaling pathway to explore its antineoplastic mechanisms. Methods：Breast cancer cell lines MCF-7 and MDA-MB-231 were treated with D-Rhamnose β hederin at different concentrations. Apoptosis rate of MCF-7 and MDA-MB-231 after treated with D- Rhamnose β hederin for 48 h were analyzed by AnnexinV/Pl double staining of flow cytometry. Protein expression of PI3K/AKT signaling pathway related molecules after treated with D-Rhamnose β hederin were detected by Western blot. Results：D-Rhamnose β hederin with dosage of 20,30,40 μg/ml effectively induced cell apoptosis and the apoptosis rate was increased with the rising concentration. After treatment with 20 μg/ml D-Rhamnose β hederin for 48 h,the protein expressions of p-PI3K and p-AKT were decreased,but the total expressions of PI3K and AKT were not significantly changed. Futhermore,PI3K inhibitor LY294002 enhanced D-Rhamnose β hederin-induced apoptosis through inhibition of p-AKT. Conclusion： D-Rhamnose β hederin could effect on the expression of AKT phosphorylation and significantly induce the apoptpsis of breast cancer cells by inhibiting the phosphorylation of PI3K.