异丙酚通过调控PI3K/AKT通路对胶质瘤U87细胞增殖、凋亡的影响  

Effects of propofol on proliferation and apoptosis of glioma U87 cells by regulating PI3K/AKT pathway

作　　者：李洪军[1] 余云明[1] 阳兴[1] 周文[1] 李明 LI Hong-jun;YU Yun-ming;YANG Xing;ZHOU Wen;LI Ming(Department of Anesthesiology,Chongqing Three Gorges Central Hospital,Chongqing 404000,China)

机构地区：[1]重庆三峡中心医院麻醉科,重庆404000

出　　处：《实用药物与临床》2020年第8期704-708,共5页Practical Pharmacy and Clinical Remedies

摘　　要：目的研究异丙酚对胶质瘤U87细胞增殖、凋亡的影响,并初步分析其机制。方法体外培养胶质瘤U87细胞,利用不同浓度异丙酚处理细胞,实验分组:空白对照组(BC组)、P1组(异丙酚浓度为0.01 mmol/L)、P2组(异丙酚浓度为0.02 mmol/L)、P3组(异丙酚浓度为0.05 mmol/L)。采用CCK-8法检测细胞增殖情况,采用平板克隆实验检测细胞增殖情况,采用流式细胞仪检测细胞凋亡,划痕实验检测细胞迁移情况,Transwell实验检测细胞侵袭情况,利用Western blot检测Ki67、Caspase-9、MMP-9蛋白、3-磷酸肌醇激酶(PI3K)、磷酸化-PI3K(p-PI3K)、蛋白质丝氨酸苏氨酸蛋白激酶(AKT)、磷酸化-AKT(p-AKT)相对表达量。结果不同浓度异丙酚处理后,P1、P2、P3组胶质瘤U87细胞增殖率、细胞平板克隆形成率、细胞迁移率、侵袭细胞数较BC组均显著降低,凋亡率升高(P<0.05),随着异丙酚浓度升高,U87细胞增殖率、细胞平板克隆形成率、细胞迁移率、侵袭细胞数显著降低,凋亡率显著升高(P<0.05)。不同浓度异丙酚处理后,P1、P2、P3组细胞p-PI3K、p-ATK蛋白表达量显著降低(P<0.05),且随异丙酚浓度升高,p-PI3K、p-ATK蛋白表达量逐渐降低(P<0.05);异丙酚处理前后PI3K、ATK蛋白表达量比较差异无统计学意义(P>0.05)。结论异丙酚可能通过抑制PI3K/AKT通路,进而抑制胶质瘤U87细胞增殖、侵袭和迁移,促进细胞凋亡。Objective To study the effects of propofol on the proliferation and apoptosis of glioma U87 cells,and to analyze its mechanism preliminarily.Methods U87 glioma cells were cultured in vitro and treated with different concentrations of propofol,and then the cells were divided into blank control group(BC group),P1 group(0.01 mmol/L propofol),P2 group(0.02 mmol/L propofol),and P3 group(0.05 mmol/L propofol).CCK-8 method was used to detect cell proliferation.Cell proliferation was detected by plate cloning assay;cell apoptosis was detected by flow cytometry;scratch test was used to detect cell migration;Transwell assay was used to detect cell invasion;the relative expressions of Ki67,Caspase-9,MMP-9,3-phosphate inositol kinase(PI3K),phosphorylated-PI3K,protein serine threonine protein kinase(AKT)and phosphorylated-AKT were detected by Western blot.Results After treatment with different concentrations of propofol,the proliferation rate,cell plate cloning rate,cell migration rate and invasive cell number of glioma U87 cells in P1,P2 and P3 groups were significantly lower than those in BC group,and the apoptosis rate was increased(P<0.05).With the increase of propofol concentration,U87 cell proliferation rate,cell plate cloning rate,cell migration rate,and the number of invasive cells were decreased significantly(P<0.05),while the apoptotic rate was increased significantly(P<0.05).The expressions of p-PI3K and p-ATK in P1,P2 and P3 groups were decreased significantly after propofol treatment(P<0.05),and the expressions of p-PI3K and p-ATK were decreased gradually with the increase of propofol concentration(P<0.05).There was no significant difference in the expressions of PI3K and ATK before and after treatment with propofol(P>0.05).Conclusion Propofol can inhibit the proliferation,invasion and migration of glioma U87 cells and promote cell apoptosis by inhibiting PI3K/AKT pathway.

关 键 词：胶质瘤 异丙酚 细胞增殖 细胞凋亡 细胞侵袭 

分 类 号：R739.41[医药卫生—肿瘤]