五味子甲素协同吉西他滨调控β-catenin通路抑制胰腺癌细胞增殖的研究

Study on the synergistic inhibitory effect of deoxyschizandrin and gemcitabine on pancreatic cancer cell proliferation via regulatingβ-catenin pathway

目的研究五味子甲素协同吉五味子甲素抑制胰腺癌细胞增殖的作用及机制。方法培养胰腺癌PANC-1细胞株,用50μg/mL吉西他滨、25μmol/L五味子甲素或50μg/mL吉西他滨联合25μmol/L五味子甲素处理,检测细胞活力、细胞周期及B淋巴细胞瘤-2基因(Bcl-2)、Bcl-2相关X蛋白(Bax)、细胞周期素D1(cyclinD1)、β-连环蛋白(β-catenin)、磷酸化糖原合成酶激酶3β(p-GSK-3β)的表达。结果与对照组比较,吉西他滨组、五味子甲素组、吉西他滨+五味子甲素组的A 490水平、细胞周期S期、G2/M期比例、Bcl-2、cyclinD1、β-catenin、p-GSK-3β的表达水平均明显降低,Bax的表达水平均明显增加(P<0.05)吉西他滨+五味子甲素组的A 490水平、细胞周期S期、G2/M期比例、Bcl-2、cyclinD1、β-catenin、p-GSK-3β的表达水平均明显低于吉西他滨组、五味子甲素组,Bax的表达水平均明显高于吉西他滨组、五味子甲素组。结论五味子甲素具有协同吉西他滨抑制胰腺癌细胞增殖的作用,该作用可能与靶向抑制β-catenin通路有关应补充抑制和刺激实验。

Objective To study the synergistic inhibitory effect of deoxyschizandrin and gemcitabine on pancreatic cancer cell proliferation and its mechanism.Methods PANC-1 cell line was cultured and treated with 50μg/ml gemcitabine,25μmol/L deoxyschizandrin or 50μg/ml gemcitabine combined with 25μmol/L deoxyschizandrin.Then cell viability,cell cycle,the expression of Bcl-2,Bax,cyclinD1,β-catenin,p-GSK-3βwere detected.Results Compared with the control group,the levels of A490,the proportion of S phase and G2/M phase,the expression of Bcl-2,Bax,cyclinD1,β-catenin,p-GSK-3βin gemcitabine group,deoxyschizandrin group,gemcitabine+deoxyschizandrin group significantly decreased,the expression of Bax significantly increased(P<0.05)and the levels of A490,the proportion of S phase and G2/M phase,the expression of Bcl-2,cyclinD1,β-catenin,p-GSK-3βin gemcitabine+deoxyschizandrin group were significantly lower than gemcitabine group,deoxyschizandrin group,the expression of Bax was significantly higher than gemcitabine group,deoxyschizandringroup.Conclusion Deoxyschizandrin there is synergistic effect with gemcitabine on the inhibition of pancreatic cancer cells proliferation,which may relate to the targeted inhibition ofβ-catenin pathway.