摘要
目的探讨柯里拉京能否通过下调NOTCH1信号通路抑制胃癌SGC-7901细胞的增殖,以及对Hes1表达的影响。方法使用不同浓度的柯里拉京(0μg/ml、10μg/ml和100μg/ml)对胃癌SGC-7901细胞进行干预。在不同时间点(0、24和48h)使用MTT法对SGC-7901细胞活性进行检测。干预48h后,使用qPCR和western blot对在不同浓度(0μg/ml、10μg/ml和100μg/ml)柯里拉京干预后,细胞NOTCH1、Hes1mRNA和蛋白的表达水平进行分析。结果使用不同浓度柯里拉京(0μg/ml、10μg/ml和100μg/ml)对胃癌SGC-7901细胞进行干预后,细胞活性呈时间依赖性和剂量依赖性下降,差异均有统计学意义(P<0.05)。不同浓度柯里拉京(0μg/ml、10μg/ml和100μg/ml)干预48h后,胃癌SGC-7901细胞NOTCH1及Hes1 mRNA和蛋白的表达水平呈剂量依赖性降低,差异均有统计学意义(P<0.05)。结论柯里拉京可通过下调NOTCH1/Hes1信号通路抑制胃癌SGC-7901细胞增殖,同时为柯里拉京用于临床治疗胃癌等恶性肿瘤奠定了实验基础。
Objective To explore whether corilagin would suppress the proliferation of gastric cancer SGC-7901 cells through mediation of NOTCH1/Hesl pathway. Methods Three different concentrations （0μg/ml, 10μg/ml and 100μg/ml） of corilagin were obtained in our study. At different time points （0h, 24h and 48h）, MTT assay was used to analyze the cell viabilities. QPCR was used to measure NOTCH1 and Hesl mRNA expression. Western blot was performed to analyze the protein expression of NOTCH1 and Hesl. Results The cell viabilities of gastric cancer SGC-7901 ceils were concentration-dependently and time-dependently supressed by corilagin. Then, the mRNA and protein expression of NOTCH1 and Hesl were also concentration-dependently inhibited by corilagin in gastric cancer SGC-7901 cells, after 48h of intervention. Conclusion Corilagin could suppress the proliferation of gastric cancer SGC-7901 cells through down-regulation of NOTCH1/Hes1 signal pathway.
出处
《西部医学》
2018年第2期178-181,共4页
Medical Journal of West China
基金
南京军区面上项目科研课题(15MS072)
