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Related Experiment Video

Updated: Nov 2, 2025

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue
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Early glycolytic reprogramming controls microglial inflammatory activation.

Junjie Cheng1, Rong Zhang1, Zhirou Xu1

  • 1Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, Jiangsu, China.

Journal of Neuroinflammation
|June 10, 2021
PubMed
Summary
This summary is machine-generated.

Inhibiting glycolysis, a metabolic process, reduces microglial activation and neuroinflammation. This finding suggests targeting glycolysis could treat neurodegenerative diseases like Parkinson's disease.

Keywords:
2-DGGlycolytic inhibitorsMicroglial cellsNF-κBNeuroinflammation

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Area of Science:

  • Neuroscience
  • Immunology
  • Metabolism

Background:

  • Neuroinflammation, driven by microglial activation, is key in neurodegenerative diseases.
  • Microglial inflammatory activation involves a metabolic shift towards aerobic glycolysis.
  • The precise role of glycolysis in microglial activation and neuroinflammation requires further elucidation.

Purpose of the Study:

  • To investigate the role of glycolysis in microglial activation and neuroinflammation.
  • To explore the anti-inflammatory and neuroprotective mechanisms of glycolysis inhibition.
  • To evaluate the therapeutic potential of glycolysis inhibitors in Parkinson's disease models.

Main Methods:

  • In vitro studies utilized LPS-activated BV-2 and primary microglial cells.
  • Assays included ELISA, RT-PCR, Western blot, immunoprecipitation, flow cytometry, and NF-κB luciferase reporter assays.
  • In vivo studies employed MPTP- and LPS-induced Parkinson's disease models, assessing neuroprotection via immunofluorescence, behavior tests, and Western blot.

Main Results:

  • LPS-induced microglial activation and glycolysis were inhibited by glycolysis inhibitors (2-DG, 3-BPA) and siRNAs targeting Glut-1 and HK2.
  • Glycolysis inhibition suppressed key inflammatory pathways, including mTOR, IKKβ, IκBα degradation, and NF-κB p65 nuclear translocation and activity.
  • 2-DG reduced LPS-induced p65 acetylation, mediated by SIRT1, and decreased microglial cytotoxicity towards dopaminergic neurons.
  • In vivo, 2-DG ameliorated neuroinflammation, dopaminergic cell loss, and microglial activation in both LPS- and MPTP-induced Parkinson's disease models.

Conclusions:

  • Glycolysis is a critical mediator of microglial activation.
  • Inhibiting glycolysis demonstrates significant anti-inflammatory and neuroprotective effects.
  • Targeting glycolysis presents a promising therapeutic strategy for neuroinflammatory diseases, including Parkinson's disease.