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NPPB 对人脑胶质瘤 SHG-44细胞凋亡的诱导作用及其机制

田晶 齐玲 纪朋艳 沈楠 崔万丽 王春艳

吉林大学学报(医学版)2016,Vol.42Issue(4):637-641,5.
吉林大学学报(医学版)2016,Vol.42Issue(4):637-641,5.DOI:10.13481/j.1671-587x.20160401

NPPB 对人脑胶质瘤 SHG-44细胞凋亡的诱导作用及其机制

Induction effect of NPPB on apoptosis of human glioma SHG-44 cells and its mechanism

田晶 1齐玲 2纪朋艳 3沈楠 3崔万丽 1王春艳1

作者信息

  • 1. 吉林医药学院生理学教研室,吉林 吉林 132013
  • 2. 吉林医药学院病理学教研室,吉林 吉林 132013
  • 3. 吉林医药学院实验中心,吉林 吉林 132013
  • 折叠

摘要

Abstract

Objective:To investigate the induction effect of NPPB,a chloride channel blocker,on the apoptosis of human glioma SHG-44 cells,and to explore its mechanism. Methods:The SHG-44 cells were cultured in vitro and divided into control group and NPPB groups (50,100,200 μmol· L-1 ).The cell viability was detected by MTT assay.The apoptotic rates were detected by flow cytometry.The expression levels of Bax, Bcl-2 and caspase-3 were detected by immunohistochemical analysis and Western blotting method.Results:Compared with control group,the cell viabilities of SHG-44 cells in 100 and 200 μmol·L-1 NPPB groups after treated for 24 and 48 h were decreased significantly (P < 0.01).The results of flow cytometry showed that the apoptotic rates of SHG-44 cells in 100 and 200 μmol·L-1 NPPB groups were 24.64% and 41.85%,and they were higher than that in control group (4.17%) (P <0. 01).The immunohistochemical analysis and Western blotting results showed that the expression levels of caspase-3 and Bax proteins in SHG-44 cells in 100 μmol · L-1 NPPB group were increased (P < 0.05 or P < 0. 01 ), and the expression level of Bcl-2 protein was decreased (P < 0.05 ). Conclusion:NPPB could induce the apoptosis of human glioma SHG-44 cells by the down-regulation of the expression of Bcl-2 and the up-regulation of the expression of Bax,and the activation of caspase-3.

关键词

氯通道/神经胶质瘤/细胞增殖/细胞凋亡

Key words

chloride channel/glioma/cell proliferation/apoptosis

分类

医药卫生

引用本文复制引用

田晶,齐玲,纪朋艳,沈楠,崔万丽,王春艳..NPPB 对人脑胶质瘤 SHG-44细胞凋亡的诱导作用及其机制[J].吉林大学学报(医学版),2016,42(4):637-641,5.

基金项目

国家自然科学基金资助课题(81201671);吉林省教育厅“十二五”科研项目资助课题 ()

吉林大学学报(医学版)

OA北大核心CSCDCSTPCD

1671-587X

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