中国临床解剖学杂志 ›› 2018, Vol. 36 ›› Issue (6): 626-631.doi: 10.13418/j.issn.1001-165x.2018.06.006

• 实验研究 • 上一篇    下一篇

丙泊酚对人胶质瘤U251细胞株增殖、凋亡、侵袭和转移能力的调节作用

赵华宇1, 霍树平2, 刘彦辉1, 康书峰3   

  1. 1.河北医科大学第三医院友谊院区麻醉科,  石家庄   050051;   2.河北医科大学第三医院中山院区麻醉科, 石家庄    050000;
    3.河北医科大学第三医院湘江院区麻醉科, 石家庄   050035
  • 收稿日期:2018-05-11 出版日期:2018-11-25 发布日期:2018-12-29
  • 通讯作者: 康书峰,硕士,主治医师,Tel:13363113936,E-mail:ksf200238@163.com
  • 作者简介:赵华宇(1975-),本科,主治医师,研究方向:麻醉,Tel:18932920505,E-mail:heyumy1974@sina.com
  • 基金资助:

    河北省科技厅重大项目(12966116d)

The regulatory effects of propofol on cell proliferation, apoptosis, invasion and migration of human glioma cell line U251

ZHAO Hua-yu1, HUO Shu-ping2, LIU Yan-hui 1, KANG Shu-feng3   

  1. 1. Department of Anesthesiology, friendship hospital, Third Hospital of Hebei Medical University, Shijiazhuang  050051;  2. Department of Anesthesiology, Zhongshan hospital, Third Hospital of Hebei Medical University, Shijiazhuang  050000;  3. Department of Anesthesiology, Xiangjiang hospital, Third Hospital of Hebei Medical University,  Shijiazhuang  050035, China
  • Received:2018-05-11 Online:2018-11-25 Published:2018-12-29

摘要:

目的 探究丙泊酚对人胶质瘤U251细胞增殖、凋亡、侵袭和转移能力的作用和机制。  方法    将细胞随机分为U251组、Propofol(1 mM)组、Propofol(2 mM)组和Propofol(5 mM)组。除U251组外,其余组用相应浓度的丙泊酚处理,CCK8检测细胞增殖,流式检测细胞凋亡,Transwell检测细胞侵袭能力,划痕实验检测细胞迁移能力,Western blot检测Ki67、Caspase-3、血管内皮生长因子(Vascular endothelial growth factor,  VEGF)、磷脂酰肌醇-3-羟激酶(Phosphoinositide 3-kinase, PI3K)、Akt、p-PI3K和p-Akt的表达。  结果    与U251组比较,Propofol (1, 2, 5 mM)组细胞增殖速度明显降低,细胞凋亡率显著升高;同时,Propofol (1, 2, 5 mM) 组侵袭细胞数与U251组比较明显减少,Propofol(2, 5 mM) 组划痕闭合率明显低于U251组;此外,丙泊酚还能显著抑制细胞增殖和迁移相关蛋白Ki67和VEGF表达,诱导细胞凋亡相关蛋白Caspase-3表达;丙泊酚能明显降低p-PI3K/PI3K和p-Akt/Akt的比值。  结论    丙泊酚能降低胶质瘤U251细胞的增殖、侵袭和转移能力,抑制U251细胞凋亡,作用机制可能与抑制PI3K/Akt信号通路激活有关。

关键词: 丙泊酚,  胶质瘤,  增殖,  凋亡,  侵袭,  迁移

Abstract:

Objective To investigate the effects and mechanism of propofol on cell proliferation, apoptosis, invasion and migration of human glioma cell line U251.   Methods Cells were divided into Propofol (1 M), Propofol (2 M) and Propofol (5 M) group and treated with propofol bisides U251 group. Cell proliferation was determined by CCK8 assay, flow cytometry was performed for cell apoptosis. The invasion and migration abilities of U251 cell were determined by Transwell and wound healing assays. The expressions of Ki67, Caspase-3, vascular endothelial growth factor (VEGF), phosphoinositide 3-kinase (PI3K), Akt, p-PI3K and p-Akt were measured by western blot.  Results Compared with U251 group, the cell growth rate was decreased and cell apoptosis rate was increased in Propofol (1, 2, 5 M) groups. Meanwhile, the invasion cells in the propofol (1, 2, 5 M) groups were decreased compared with the U251 group, and wound closure rate was also down-regulated in the propofol (2, 5 M) groups. In addition, propofol inhibited the expressions of Ki67 and VEGF (proliferation- and migration-related proteins) and induced expression of apoptosis-related protein Caspase-3. Propofol also decreased the ratio of p-PI3K/PI3K and p-Akt/Akt significantly. Conclusions Propofol reduces the abilities of cell proliferation, invasion and migration of glioma cell line U251 and induces cell apoptosis, the mechanism of which may be related to inhibition of the activation of PI3K/Akt signaling pathway

Key words:  Propofol; Glioma; Proliferation; Apoptosis,  Invasion; Migration