摘要
目的:采用体外培养人肝癌HepG2细胞为研究对象,探讨党参多糖(CPP)对HepG2细胞生长和运动能力的影响及其机制。方法:用不同浓度(0、0.1、0.25、0.5、1、2.5、5、10、20、50、100、200、300和400μmol/L)党参多糖作用于体外培养的人肝癌HepG2细胞,采用CCK-8法检测细胞存活率,选择5,10和20μmol/L进行后续实验。流式细胞术检测细胞凋亡率;划痕实验检测细胞迁移;Transwell检测细胞侵袭;Western blot检测上皮标志蛋白E-钙黏蛋白(E-cadherin)和间质标志蛋白N-钙黏蛋白(N-cadherin)N-cadherin、波形蛋白(Vimentin)的表达水平以及信号通路磷脂酰肌醇3-激酶(PI3K)、AKT的磷酸化情况;最后,20μmol/L党参多糖或PI3K激活剂740Y-P单独使用或联用处理HepG2细胞,检测细胞增殖、凋亡、迁移、侵袭和PI3K/AKT信号通路磷酸化。结果:党参多糖能促进体外培养HepG2细胞凋亡,抑制细胞增殖、迁移和侵袭能力;同时调节E-cadherin、N-cadherin、Vimentin和PI3K/AKT相关蛋白表达;最后,20μmol/L党参多糖和740Y-P联用能有效逆转740Y-P对细胞增殖、凋亡、侵袭和迁移能力的调节作用。结论:党参多糖能有效抑制人肝癌HepG2细胞的生长和运动能力,其机制与调节PI3K/AKT信号通路有关。
Objective:To investigate the effects of Codonopsis pilosum polysaccharide(CPP) on the growth and motility ability of HepG2 cells cultured in vitro and its mechanism.Methods:HepG2 cells cultured in vitro were treated with CPP at different concentrations(0,0.1,0.25,0.5,1,2.5,5,10,20,50,100,200,300 and 400 μmol/L).CCK-8 method was used to detect the cell viability,5,10 and 20 μmol/L were selected for subsequent experiments.Flow cytometry was used to detect apoptotic rate.Scratch test was used to detect cell migration.Transwell was used to detect cell invasion.Western blot was used to detect the expression of E-cadherin,N-cadherin and Vimentin,and the phosphorylation of PI3 K and AKT signaling pathways.Finally,after treated with 20 μmol/L CPP or PI3 K activator 740 Y-P alone or in combination,we detected cell proliferation,apoptosis,migration,invasion and phosphorylation of PI3 K/AKT signaling pathway.Results:CPP could promote apoptosis of HepG2 cells in vitro,inhibit cell proliferation,migration and invasiveness,and regulate the expression of E-cadherin,N-cadherin,Vimentin and PI3 K/AKT related proteins.Finally,the combination of 20 μmol/L CPP and 740 Y-P could effectively reverse the regulation of 740 Y-P on cell proliferation,apoptosis,invasion and migration of HepG2 cells.Conclusion:Codonopsis pilosula polysaccharide can effectively inhibit the growth and motility of human hepatocellular carcinoma HepG2 cells.Its mechanism is related to the regulation of PI3 K/AKT signaling pathway.
作者
刘云鹤
蔡金保
王红丽
LIU Yun-He;CAI Jin-Bao;WANG Hong-Li(Department of Internal Medicine-Oncology,First Affiliated Hospital of Nanyang Medical College of Henan Province,Nanyang 473000,China)
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2020年第9期1108-1113,共6页
Chinese Journal of Immunology
关键词
肝癌
党参多糖
生长
运动
740Y-P
PI3K/AKT
Hepatocellular carcinoma
Codonopsis pilosula polysaccharide
Growth
Motility
740Y-P
PI3K/AKT
作者简介
刘云鹤,女,主治医师,主要从事肿瘤内科疾病的研究。
