Related Experiment Video

Updated: Feb 13, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

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Evodiamine activates cellular apoptosis through suppressing PI3K/AKT and activating MAPK in glioma

Rong Wang1,2, Danni Deng2, Naiyuan Shao1

  • 1Department of Neurosurgery, The First People's Hospital of Changzhou, Changzhou, Jiangsu, China.

Oncotargets and Therapy
|March 15, 2018
PubMed
Abstract

Insights

Evodiamine (Evo) effectively inhibits glioblastoma multiforme (GBM) cell proliferation and induces apoptosis. This natural compound shows promise as a novel therapeutic agent for treating this aggressive brain cancer.

Area of Science:

  • Neuro-oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Glioblastoma multiforme (GBM) is a highly aggressive primary brain tumor with a poor prognosis.
  • Current treatments, including radiotherapy and temozolomide, offer limited improvements.
  • Novel therapeutic agents are urgently needed for GBM treatment.

Purpose of the Study:

  • To investigate the anti-tumor effects of evodiamine (Evo) on GBM cells.
  • To elucidate the molecular mechanisms underlying Evo's anti-cancer activity in GBM.

Main Methods:

  • MTT assays were used to assess cell proliferation inhibition.
  • Fluorescence microscopy and flow cytometry analyzed Evo-induced apoptosis.
  • Reactive oxygen species (ROS) production and mitochondrial membrane potential (MMP) were evaluated.
  • Western blotting assessed signaling pathways (PI3K/AKT, MAPK) and apoptotic protein expression.

Main Results:

  • Evodiamine significantly inhibited GBM cell proliferation in a time- and dose-dependent manner.
  • Evo induced apoptosis, increased ROS production, and disrupted MMP in GBM cells.
  • Evo suppressed PI3K/AKT signaling, activated MAPK (p38, JNK), and modulated apoptotic proteins (Bax, Bcl-2, Cytochrome c, Caspase-3, PARP).

Conclusions:

  • Evodiamine exhibits anti-tumor activity against GBM by inducing apoptosis.
  • The mechanism involves PI3K/AKT pathway suppression and MAPK activation.
  • Evodiamine represents a potential new therapeutic strategy for GBM treatment.
Keywords:
AktMAPKapoptosisevodiamineglioma

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