马齿苋结合态多酚和自由态多酚抑制肝癌细胞HepG-2增殖及诱导细胞凋亡的研究  

The proliferation inhibition and apoptosis effects of bound polyphenol and free polyphenol fromportulaca oleracea L.on human hepatoma cell line HepG-2

作　　者：王浩毓 赵惠玲[2] 李宏全[1] Wang Haoyu;Zhao Huiling;Li Hongquan(College of Animal Science and Veterinary Medicine, Shanxi Agricultural University, Jinzhong 030801, China;TaiyuanNormal University, Taiyuan 030012, China)

机构地区：[1]山西农业大学动物科技学院,山西太谷030801 [2]太原师范学院生物系,山西太原030012

出　　处：《山西农业大学学报（自然科学版）》2019年第4期70-78,共9页Journal of Shanxi Agricultural University(Natural Science Edition)

摘　　要：[目的]研究马齿苋结合态多酚和自由态多酚抑制肝癌细胞HepG-2增殖并诱导细胞凋亡的作用。[方法]将不同浓度马齿苋结合态多酚和自由态多酚与HepG-2细胞在体外培养,采用MTT检测细胞增殖活性;光镜观察细胞形态;流式细胞术分别检测细胞周期、细胞凋亡和线粒体膜电位;酶标仪检测Caspase酶活力。[结果]结果表明,马齿苋多酚对肝癌细胞HepG-2的增殖抑制作用和凋亡促进作用与一定范围的处理浓度和处理时间呈正相关,36h、0.4g·L^-1处理条件下,马齿苋自由态多酚对HepG-2细胞的抑制率仅为15.7%,而马齿苋结合态多酚对HepG-2细胞的抑制率达到73.8%;马齿苋结合态多酚作用下,HepG-2肝癌细胞光镜下可观察到细胞出现明显的形态学改变,处理后细胞周期阻滞于S期,Caspase-3、Caspase-8、Caspase-9酶活性也显著提高,并诱导细胞发生凋亡。马齿苋结合态多酚可能通过激活膜受体通路和线粒体介导的内源性凋亡通路诱导HepG-2细胞凋亡。[Objective]The present study was undertaken to analyze the induced apoptosis and proliferation inhibition influence of bound polyphenoland freepolyphenol in Portulaca Oleracea L. to HepG-2 liver cancer cells.[Methods]Different concentration of the bound polyphenol in Portulaca Oleracea L.(BPPO) and free polyphenol in Portulaca Oleracea L.(FPPO) was used to in vitro cultured with HepG-2 liver cancer cell line. The cell proliferation activity was analyzed by MTT;the cell morphology was observed by light microscope;the cell cycle, apoptosis and mitochondrial membrane potential assay were analyzed by flow cytometry;and the caspases enzymatic activity assay was analyzed by microplate reader.[Conclusion]The result showed that BPPO significantly inhibited the proliferation of HepG-2 cells in a concentration-and time-dependent manner. Significant morphological change in cells could be observed under the microscope. After treatment with BPPO, the cell cycle of HepG-2 cells was stopped in S phase, and the enzyme activity of caspase3,caspase 8 and caspase 9 were also significantly increased. In summary, the BPPO could significantly inhibit the proliferation and induce apoptosis of HepG-2 cells in a dose-and time-dependent manner, and might induce apoptosis of HepG2 cells by activating membrane receptor pathway and mitochondrial pathway.

关 键 词：马齿苋结合态多酚(BPPO) HepG-2人肝癌细胞 抗癌 细胞增殖抑制 诱导细胞凋亡 

分 类 号：S857.4[农业科学—临床兽医学]