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作 者:陈龙云 柳叶 CHEN Long-yun;LIU Ye(Basic Medical College,Hubei University of Chinese Medicine,Wuhan 430065,China;School of Laboratory Medicine,Hubei University of Chinese Medicine,Wuhan 430065,China)
机构地区:[1]湖北中医药大学基础医学院,湖北武汉430065 [2]湖北中医药大学检验学院,湖北武汉430065
出 处:《中国病理生理杂志》2018年第11期1976-1980,共5页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.31700152);湖北中医药大学青苗计划(No.2016ZZX023; No.XJ2014KJ014)
摘 要:目的:探讨槲皮苷是否通过抑制PI3K/AKT信号通路诱导人胃癌SGC7901细胞凋亡。方法:选取SGC7901细胞作为研究对象,采用MTT法检测槲皮苷对SGC7901细胞的毒性作用并测定IC50值。实验分为对照组(不加药处理)、槲皮苷组(采用200μmol/L槲皮苷处理)、PI3K/AKT通路激动剂胰岛素样生长因子1(IGF-1)组(采用100μg/L IGF-1处理)和槲皮苷+IGF-1组(采用200μmol/L槲皮苷+100μg/L IGF-1共处理)。处理48 h后,采用流式细胞术检测细胞凋亡,Western blot法检测cleaved caspase-3、p-AKT(Ser473)、AKT、p-PI3K(Tyr508)和PI3K的蛋白水平。结果:从100μmol/L开始,随着槲皮苷处理浓度的逐渐升高,SGC7901细胞活力显著降低(P <0. 05),槲皮苷作用48 h的IC50值为275. 40μmol/L。200μmol/L槲皮苷作用SGC7901细胞48 h后,与对照组比较,细胞凋亡率和cleaved caspase-3蛋白水平显著上升(P <0. 05),p-AKT和p-PI3K蛋白水平显著降低(P <0. 05),然而IGF-1与槲皮苷共同作用时,IGF-1可逆转槲皮苷对SGC7901细胞的作用效果。结论:槲皮苷能够诱导胃癌SGC7901细胞凋亡,其作用机制可能与抑制PI3K/AKT信号通路的激活有关。AIM:To investigate whether quercitrin induces apoptosis of gastric cancer cell line SGC7901 by inhibition of PI3K/AKT signaling pathway.METHODS:The human gastric cancer SGC7901 cells were selected as the research object.The cytotoxicity of quercitrin was detected by MTT assay,and IC 50 value of quercitrin was calculated.The SGC7901 cells were divided into control group,quercitrin group(incubated with 200μmol/L quercitrin),insulin-like growth factor-1(IGF-1)group(incubated with 100μg/L IGF-1)and quercitrin+IGF-1 group(incubated with 200μmol/L quercitrin and 100μg/L IGF-1).After 48 h,the apoptosis of SGC7901 cells was analyzed by flow cytometry,and the protein levels of cleaved caspase-3,p-AKT(Ser473),AKT,p-PI3K(Tyr508)and PI3K were determined by Western blot.RESULTS:The viability of SGC7901 cells was significantly decreased as the concentration of quercitrin increased,starting at 100μmol/L(P<0.05).The IC 50 value of quercitrin for 48 h was 275.40μmol/L.After treatment with 200μmol/L quercitrin for 48 h,the apoptosis rate and the protein level of cleaved caspase-3 in quercitrin group were significantly increased(P<0.05),and the phosphorylated levels of AKT and PI3K were significantly decreased compared with control group(P<0.05).Treatment with quercitrin and IGF-1 inhibited the effect of quercitrin on SGC7901 cells compared with quercitrin group.CONCLUSION:Quercitrin may induce apoptosis of gastric cancer cell line SGC7901 by inhibiting the activation of PI3K/AKT signaling pathway.
关 键 词:槲皮苷 胃癌 细胞凋亡 PI3K/AKT信号通路
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