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雷公藤多苷对人口腔癌KB细胞增殖、凋亡及PI3K/AKT信号通路的影响 被引量:12

Effects of tripterygium wilfordii polyglycosides on the proliferation,apoptosis and PI3K/AKT signaling pathway of human oral cancer KB cells
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摘要 目的探讨雷公藤多苷对人口腔癌KB细胞增殖、凋亡和PI3K/AKT信号通路的影响。方法将对数生长期的人口腔癌KB细胞分为空白对照组和20μmol/L、40μmol/L、80μmol/L、160μmol/L雷公藤多苷给药组。分别采用CCK-8法检测细胞增殖抑制率,流式细胞术检测细胞凋亡率,Westernblot检测人口腔癌KB细胞磷酸化PI3K(p-PI3K)和磷酸化AKT(p-AKT)蛋白的表达水平。结果雷公藤多苷对人口腔癌KB细胞的增殖有明显的抑制作用,并促进细胞凋亡。与对照组比较,雷公藤多苷给药组人口腔癌KB细胞中p-PI3K和p-AKT蛋白表达水平明显降低。结论雷公藤多苷具有抑制人口腔癌KB细胞增殖和诱导其凋亡作用,其机制可能与抑制PI3K/AKT信号通路的激活有关。 Objective To investigate the effect of tripterygium wilfordii polyglycosides on the proliferation,apoptosis and PI3K/AKT signaling pathway of human oral cancer KB cells.Methods Human oral cancer KB cells with logarithmic growth stage were divided into the control group and different drug groups with 20μmol/L,40μmol/L,80μmol/L,160μmol/L of tripterygium wilfordii polygl ycosides.The inhibition rate of cell proliferation was detected by CCK-8 method,apoptosis rate was detected by flow cytometry,and the expression levels of p-PI3K and p-AKT in KB cells were detected by Western blot.Results Tripterygium wilfordii polyglycoside significantly inhibited the proliferation of KB cells,and promoted cell apoptosis.Compared with the control group,the expression levels of p-PI3K and p-AKT in KB cells treated by the tripterygium wilfordii polyglycoside were significantly decreased.Conclusion Tripterygium wilfordii polyglycosides can inhibit the proliferation and induce the apoptosis of human oral cancer KB cells.The mechanism may be related to inhibition of activation of PI3K/AKT signaling pathway.
作者 厉婷 周和超 陈驹 LI Ting;ZHOU Hechao;CHEN Ju(Department of Pharmacy,Affiliated Hospital of Guangdong Medical University,Zhanjiang 524001,China;Cancer Center,Affiliated Hospital of Guangdong Medical University,Zhanjiang 524001,China)
出处 《广东药科大学学报》 CAS 2019年第5期653-657,共5页 Journal of Guangdong Pharmaceutical University
关键词 雷公藤多苷 口腔癌 PI3K/AKT信号通路 增殖 凋亡 tripterygium wilfordii polyglycosides oral cancer PI3K/AKT signaling pathway proliferation apoptosis
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