裂果薯总皂苷对大鼠肝卵圆细胞系WB-F344上皮间质转化的影响  

The effect of total saponins of Schizocapsa plantaginea Hance on epithelial-mesenchymal transition of rat hepatic oval cell line WB-F344

作　　者：李锦华 莫宇雪 郭心怡 梁梓樱 李昊 吕美娴 王燕雪 梁钢[1,2] LI Jinhua;MO Yuxue;GUO Xinyi;LIANG Ziying;LI Hao;Lyu Meixian;WANG Yanxue;LIANG Gang(College of Pharmacy,Guangxi Medical University,Nanning 530021,China;State key Laboratory of Targeting Oncology,Nanning 530021,China)

机构地区：[1]广西医科大学药学院,南宁530021 [2]省部共建靶向肿瘤学国家重点实验室,南宁530021

出　　处：《广西医科大学学报》2024年第5期639-645,共7页Journal of Guangxi Medical University

基　　金：国家自然科学基金资助项目(No.81960737,No.82360792)。

摘　　要：目的:探讨裂果薯总皂苷(SSPHs)对转化生长因子-β1(TGF-β1)诱导的大鼠肝卵圆细胞系WB-F344上皮间质转化(EMT)的影响及作用机制。方法:将WB-F344细胞分为对照组、模型组,SSPHs低、中、高剂量组和PI3K/AKT信号通路抑制剂LY294002组。除对照组外,其余各组均以10μg/L TGF-β1诱导WB-F344构建EMT模型。采用MTT法、细胞划痕实验分别检测细胞增殖、迁移能力,实时荧光定量PCR(RT-qPCR)、western blotting法分别检测E-钙黏蛋白(E-cadherin)、N-钙黏蛋白(Ncadherin)、波形蛋白(Vimentin)的m RNA和蛋白表达,western blotting法检测PI3K/AKT信号通路关键蛋白表达。结果:SSPHs可抑制TGF-β1诱导的WB-F344细胞的增殖,24 h的细胞半数抑制浓度(IC50)为3.02μg/mL。与对照组比较,模型组N-cadherin、Vimentin的mRNA及蛋白表达水平显著升高,E-cadherin mRNA及蛋白表达水平显著降低,p-PI3K/PI3K、p-AKT/AKT比值显著升高(均P<0.05)。与模型组比较,SSPHs中、高剂量组N-cadherin和Vimentin mRNA及蛋白表达下调,E-cadherin mRNA及蛋白表达上调,p-PI3K/PI3K、p-AKT/AKT比值降低(均P<0.05),结果与LY294002组相似。结论:SSPHs可抑制TGF-β1诱导的WB-F344细胞EMT进程,其机制可能与抑制PI3K/AKT信号通路有关。Objective:To investigate the effect and mechanism of total saponins of Schizocapsa plantaginea Hance(SSPHs)on epithelial mesenchymal transformation(EMT)of rat hepatic oval cells WB-F344 induced by transforming growth factor-β1(TGF-β1).Methods:WB-F344 cells were divided into control group,model group,low-,medium-and high-dose SSPHs groups and PI3K/AKT signaling pathway inhibitor LY294002 group.Except the control group,all the other groups were induced with 10μg/L TGF-β1 to establish the EMT model.MTT assay and cell scratch assay were used to detect cell proliferation and migration.Reverse transcription-quantitative PCR(RT-qPCR)and western blotting were used to detect the mRNA and protein expression of E-cadherin,N-cadherin and Vimentin,respectively.The expression of key proteins in PI3K/AKT signaling pathway was detected by western blotting.Results:SSPHs inhibited the proliferation of TGF-β1-induced WB-F344 cells,with a half maximal inhibitory concentration(IC50)value of 3.02μg/mL at 24 hours.Compared with the control group,the model group showed significantly increased mRNA and protein expression levels of N-cadherin and Vimentin,significantly decreased mRNA and protein expression of E-cadherin,and significantly increased ratio of p-PI3K/PI3K and p-AKT/AKT(all P<0.05).Compared with the model group,N-cadherin and Vimentin mRNA and protein expression was down-regulated,E-cadherin mRNA and protein expression was upregulated,and P-PI3K/PI3K and P-AkT/AKT ratios were decreased in the THE SSPHs medium and high-dose groups(all P<0.05),with results similar to those observed in the LY294002 group(all P<0.05).Conclusion:SSPHs can inhibit the EMT process in TGF-β1-induced WB-F344 cells,and its mechanism may be related to the inhibition of PI3K/AKT signaling pathway.

关 键 词：裂果薯总皂苷 肝卵圆细胞 PI3K/AKT 上皮间质转化 肝癌前病变 转化生长因子-β1 

分 类 号：R735.7[医药卫生—肿瘤]