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莲心碱通过ROS/JNK途径诱导人胶质瘤U251细胞的凋亡

李承科 何琴 罗孝全 冯浩 谯飞

医学分子生物学杂志2025,Vol.22Issue(2):124-130,7.
医学分子生物学杂志2025,Vol.22Issue(2):124-130,7.DOI:10.3870/j.issn.1672-8009.2025.02.004

莲心碱通过ROS/JNK途径诱导人胶质瘤U251细胞的凋亡

Liensinine Induces Apoptosis in Glioma U251 Cells through ROS/JNK Pathway

李承科 1何琴 2罗孝全 1冯浩 1谯飞1

作者信息

  • 1. 首都医科大学附属北京安贞医院南充医院·南充市中心医院 神经外科,四川省 南充市,637000
  • 2. 首都医科大学附属北京安贞医院南充医院·南充市中心医院 烧伤整形与皮肤美容外科 四川省 南充市,637000
  • 折叠

摘要

Abstract

Objective To investigate the effect of liensinine(LI)on apoptosis of U251 glioma cells and its mechanisms.Methods U251 and HEB cells were treated with different concentrations of LI for 24/48 h,CCK8 assay and colony formation assay were performed to detect cell viability,flow cytometer was performed to detect apoptosis,and the expression levels of apoptotic proteins(Bax/Bcl-2,cleaved PARP)were detected by Western blotting.Cells were divided into 6 groups:control,LI,NAC,LI+NAC,SP600125,LI+SP600125.ROS was detected by DCFH-DA and p-JNK/cleaved PARP by Western blotting.U251 xenograft model was established to evaluate the effect of LI on tumor volume/weight and tumor cell apoptosis.Results LI significantly inhibited the proliferation of U251 cells,decreased the colony formation of U251 cells,and promoted apopto-sis.LI(80 μmol/L)induced ROS production and JNK phosphorylation,which were reversed by NAC and SP600125.In vivo experiments showed that LI inhibited tumor growth,reduced Ki67 posi-tive cells,and promoted apoptosis.Conclusion LI selectively inhibits U251 via ROS/JNK-media-ted apoptosis,demonstrating therapeutic potential for glioma.

关键词

胶质瘤/莲心碱/细胞凋亡/自噬/LC3B

Key words

glioma/liensinine/apoptosis/autophagy/LC3B

分类

临床医学

引用本文复制引用

李承科,何琴,罗孝全,冯浩,谯飞..莲心碱通过ROS/JNK途径诱导人胶质瘤U251细胞的凋亡[J].医学分子生物学杂志,2025,22(2):124-130,7.

基金项目

四川省科技计划项目(No.2023JDRC0091) This work was supported by a grant from the Science and Technology Pro-ject of Sichuan Province(No.2023JDRC0091) (No.2023JDRC0091)

医学分子生物学杂志

1672-8009

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