Research on the mechanism of remifentanil on the malignant biological behaviors of glioma cells

LYU Wen-jing; TANG Run-dong; LIU Kun; ZHANG Hua-shan; SI Jing-dong; ZHANG Xing-yue

doi:10.11659/jjssx.09E025070

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Research on the mechanism of remifentanil on the malignant biological behaviors of glioma cells

Basic Research | 更新时间：2026-05-25

- Research on the mechanism of remifentanil on the malignant biological behaviors of glioma cells
- JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY Vol. 35, Issue 5, Pages: 407-413(2026)
- 作者机构：
  
  1.聊城市第二人民医院麻醉科，山东聊城 252600
  2.青岛大学附属医院麻醉科，山东青岛 266000
  3.聊城市第二人民医院神经外科，山东聊城 252600
- 作者简介：
- 基金信息：
- DOI：10.11659/jjssx.09E025070
  CLC： R739.41;R971+.2
- Received：18 September 2025，
  
  Published：25 May 2026
- 稿件说明：
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吕文静,唐润栋,刘昆等.瑞芬太尼对脑胶质瘤细胞恶性生物学行为的影响机制研究[J].局解手术学杂志,2026,35(05):407-413.

LYU Wen-jing,TANG Run-dong,LIU Kun,et al.Research on the mechanism of remifentanil on the malignant biological behaviors of glioma cells[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2026,35(05):407-413.
吕文静,唐润栋,刘昆等.瑞芬太尼对脑胶质瘤细胞恶性生物学行为的影响机制研究[J].局解手术学杂志,2026,35(05):407-413. DOI： 10.11659/jjssx.09E025070.

LYU Wen-jing,TANG Run-dong,LIU Kun,et al.Research on the mechanism of remifentanil on the malignant biological behaviors of glioma cells[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2026,35(05):407-413. DOI： 10.11659/jjssx.09E025070.

摘要

目的

探讨瑞芬太尼对脑胶质瘤细胞恶性生物学行为的影响及可能机制。

方法

用0、0.5、1.0、2.0、4.0、8.0 mg/mL瑞芬太尼处理脑胶质瘤细胞U87 MG，CCK-8检测细胞活性，计算

；将U

87 MG细胞分为对照组（Control组）、瑞芬太尼组（Remifentanil组）、瑞芬太尼+Jagged-1/Notch信号通路激活剂组（Remifentanil+Jagged-1组）、Jagged-1/Notch信号通路抑制剂组（DAPT组）、瑞芬太尼+Jagged-1/Notch信号通路抑制剂组（Remifentanil+DAPT组）；细胞克隆实验检测细胞增殖能力；流式细胞术检测细胞凋亡情况；Western blot检测细胞增殖、凋亡、上皮间质转化（EMT）及Jagged-1/Notch信号通路相关蛋白表达。建立裸鼠移植瘤模型，分析瑞芬太尼对移植瘤生长及Jagged-1/Notch信号通路相关蛋白表达的影响；免疫组化检测瘤组织增殖、凋亡、EMT相关蛋白表达。

结果

与Control组比较，Remifentanil组和DAPT组细胞克隆数减少（

0.05），Ki67、PCNA、Snail、N-cadherin、Vimentin、Jagged-1、Notch1、Hes1蛋白表达降低（

0.05），细胞凋亡率、Bax、C-caspase-3表达升高（

0.05）；与Remifentanil组比较，Remifentanil+Jagged-1组细胞克隆数增加（

0.05），Ki67、PCNA、Snail、N-cadherin、Vimentin、Jagged-1、Notch1、Hes1表达升高（

0.05），细胞凋亡率，Bax、C-caspase-3蛋白表达降低（

0.05）；与Remifentanil组和DAPT组比较，Remifentanil+DAPT组细胞克隆数减少（

0.05），Ki67、PCNA、Snail、N-cadherin、Vimentin、Jagged-1、Notch1、Hes1蛋白表达降低（

0.05），细胞凋亡率，Bax、C-caspase-3蛋白表达升高（

0.05）。裸鼠移植瘤实验结果显示，与NC组比较，REM组移植瘤体积、瘤质量及Jagged-1、Notch1、Hes1、Ki67、PCNA、Snail、N-cadherin和Vimentin表达降低（

0.05），Bax、C-caspase-3表达升高（

0.05）。

结论

瑞芬太尼可抑制脑胶质瘤细胞的增殖及EMT，并促进其凋亡，该作用与抑制Jagged-1/Notch信号通路相关。

Abstract

Objective

To investigate the effects of remifentanil on malignant biological behaviors of glioma cells and its potential mechanism.

Methods

U87 MG glioma cells were treated with remifentanil at concentrations of 0， 0.5， 1.0， 2.0， 4.0， and 8.0 mg/mL. Cell viability was assessed by CCK-8 assay， and

was calculated. U87 MG cells were divided into the Control group， the Remifentanil group， the Remifentanil+Jagged-1/Notch signaling pathway activator group （the Remifentanil+Jagged-1 group）， the Jagged-1/Notch signaling pathway inhibitor group （the DAPT group）， and the Remifentanil+Jagged-1/Notch signaling pathway inhibitor group （the Remi

fentanil+DAPT group）. Cell colony formation assay was used to detect cell proliferation ability. Flow cytometry was used to detect cell apoptosis. Western blot was used to detect the expression levels of proteins related to cell proliferation， apoptosis， epithelial-mesenchymal transition （EMT）， and the Jagged-1/Notch signaling pathway. A nude mouse xenograft tumor model was established to evaluate the effects of remifentanil on tumor growth and the expression levels of proteins related to Jagged-1/Notch signaling pathway. Immunohistochemistry was used to detect the expression levels of proliferation， apoptosis， and EMT-related proteins in tumor tissues.

Results

Compared with the Control group， the number of cell colonies and the expression levels of Ki67， PCNA， Snail， N-cadherin， Vimentin， Jagged-1， Notch1 and Hes1 proteins in both the Remifentanil group and the DAPT group were decreased （

0.05）， while the apoptosis rate and the expression levels of Bax and C-caspase-3 proteins were increased （

0.05）. Compared with the Remifentanil group， the number of cell colonies and the expression levels of Ki67， PCNA， Snail， N-cadherin， Vimentin， Jagged-1， Notch1 and Hes1 proteins in the Remifentanil+Jagged-1 group were increased （

0.05）， while the apoptosis rate and the expression levels of Bax and C-caspase-3 proteins were decreased （

0.05）. Compared with the Remifentanil group and the DAPT group，the number of cell colonies and the expression levels of Ki67，PCNA，Snail，N-cadherin，Vimentin， Jagged-1， Notch1 and Hes1 proteins in the Remifentanil+DAPT group were decreased （

0.05）， while the apoptosis rate and the expression levels of Bax and C-caspase-3 proteins were increased （

0.05）. The results of the nude mouse xenograft tumor experiment showed that compared with the NC group， the tumor volume and tumor weight， as well as the expression levels of Jagged-1， Notch1， Hes1， Ki67， PCNA， Snail， N-c

adherin and Vimentin in the REM group were decreased （

0.05）， while the expression levels of Bax and C-caspase-3 were increased （

0.05）.

Conclusion

Remifentanil inhibits the proliferation and EMT and promotes apoptosis of glioma cells， and this effect is associated with the inhibition of Jagged-1/Notch signaling pathway.

关键词

Keywords

references

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