摘要
目的:探究芒柄花黄素(Formononetin,Form)对注射人胃癌细胞系SGC7901细胞悬液裸鼠的保护作用和具体机制.方法:建模成功后将裸鼠分为对照组,低、中、高浓度(10、20、40 mg/kg)芒柄花黄素处理组.观察皮下肿瘤,称量湿重,计算出肿瘤湿重抑制率及体积抑制率.Western blot法检测β-catenin、p-β-catenin、CyclinD1、CDK4 以及 p-Akt、Akt、Bcl-2、Bax、Caspase3 蛋白的相对表达量;免疫组织化学方法测定各组裸鼠肿瘤组织中β-catenin、p-β-catenin、CyclinD1、CDK4、Cas-pase3、Caspase9蛋白表达情况.结果:免疫组织化学方法结果显示β-catenin、p-β-catenin、Cy-clinD1、CDK4表达情况随Form干预浓度增加而减弱;Caspase3、Caspase9表达随Form干预浓度增加而增强.Western blot 结果显示 β-Catenin、p-β-Catenin、CyclinD1、CDK4 以及 p-Akt、Akt、Bcl-2等蛋白的相对表达量随Form干预浓度增加而降低;Caspase3、Bax等蛋白的相对表达量随Form干预浓度增加而上升.结论:Form可以通过抑制Wnt/β-catenin信号通路而抑制胃癌细胞的增殖,同时还可以上调Caspase3来促进胃癌细胞的凋亡.
Abstract
Objective:To explore the protective effect and mechanism of Formononetin(Form)on nude mice injected with human gastric cancer cell line SGC7901 cell suspension.Methods:Af-ter successful modeling,nude mice were divided into control group,low,medium and high concen-tration(10,20,40 mg/kg)ononcetin treatment group.The subcutaneous tumor was observed,the wet weight was weighed,and the wet weight inhibition rate and volume inhibition rate were calcu-lated.The relative expression levels of β-Catenin,p-β-Catenin,CyclinD1,CDK4,p-Akt,Akt,Bcl-2,Bax,Caspase3 and other proteins were detected by Western blot.The expression ofβ-catenin,p-β-catenin,CyclinD1,CDK4,Caspase3 and Caspase9 in tumor tissues of nude mice were determined by immunohistochemical method.Results:Immunohistochemical results showed that the expressions of β-catenin,p-β-catenin,CyclinD1 and CDK4 decreased with the increase of Form concentration.The expression of Caspase3 and Caspase9 increased with the increase of Form concentration.Western blot results showed that the relative expression levels of β-Catenin,p-β-Catenin,CyclinD1,CDK4,p-Akt,Akt,Bcl-2 proteins decreased with the increase of Form in-tervention concentration.The relative expression levels of Caspase3,Bax and other proteins in-creased with the increase of Form intervention concentration.Conclusion:Form can inhibit the proliferation of gastric cancer cells by inhibiting Wnt/β-catenin signaling pathway,and can also up-regulate Caspase3 to promote apoptosis of gastric cancer cells.
NETL
NSTL
维普
万方数据