甘草甜素对HepG2细胞的影响及其作用机制
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甘草甜素对HepG2细胞的影响及其作用机制
张丽娟;韩娜;丁亚文;王晓娟;冯刚
【期刊名称】《肿瘤药学》
【年(卷),期】2018(8)2
【摘要】目的研究甘草甜素在HepG2细胞恶性增殖中的作用及其分子机制.方法取对数生长期的HepG2细胞分别用50,100,200 μmol·L-1不同浓度的甘草甜素
培养12 h、24 h、48 h.采用MTT法检测甘草甜素对HepG2细胞增殖的影响;采
用TUNEL染色法和GFP-LC3质粒转染法检测甘草甜素对HepG2细胞凋亡及自
噬的影响;采用Western blot检测甘草甜素对P13K/AKT/mTOR信号通路中关键蛋白的影响.结果甘草甜素可显著抑制HepG2细胞增殖,促进细胞凋亡及细胞中自噬小体的形成.与对照组相比较,甘草甜素处理HepG2细胞48 h后,细胞中mTOR、S6、PI3K以及AKT的磷酸化水平明显降低.结论甘草甜素通过抑制
PI3K/AKT/mTOR通路诱导凋亡和自噬,进而抑制HepG2细胞的恶性增
殖.%Objective To study the role and molecular mechanism of glycyrrhizin on HepG2 cell proliferation. Methods The HepG2 cells of the logarithmic growth were used for 50, 100, 200 μmol·L-1different concentrations of glycyrrhizin, which were cultured for 12 h, 24 h and 48 h respectively. The effects of glycyrrhizin on proliferation of HepG2 cells were detected by MTT assay. The effects of glycyrrhizin on HepG2 cell apoptosis and autophagy were detected by TUNEL staining and GFP-LC3 transfection. Western blot was used to detect the influence of glycyrrhizin on key proteins in P13K/AKT/mTOR signaling pathway. Results Results from MTT
assay showed that glycyrrhizin could inhibit HepG2 cell proliferation significantly. Results from TUNEL staining also found that glycyrrhizin can significantly promote the apoptosis of HepG2 cells. Results from GFP-LC3 transfection experiment found that glycyrrhizin can significantly promote the formation of autophagy in HepG2 cells. At the same time, mTOR, S6, PI3K and AKT in the cells were significantly decreased after the treatment of HepG2 cells for 48 hours compared with that in the control group. Conclusion Glycyrrhizin inhibits the proliferation of HepG2 cells by in-hibiting the apoptosis and autophagy mediated by PI3K/AKT/mTOR pathway.
【总页数】4页(P158-161)
【作者】张丽娟;韩娜;丁亚文;王晓娟;冯刚
【作者单位】航天中心医院肿瘤科,北京,100049;航天中心医院外科,北京,100049;武汉市普爱医院肿瘤科,湖北武汉,430030;武汉市普爱医院肿瘤科,湖北武
汉,430030;武汉市普爱医院肿瘤科,湖北武汉,430030
【正文语种】中文
【中图分类】R735.7
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