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Galectin-1 attenuates neurodegeneration in Parkinson's disease model by modulating microglial MAPK/IκB/NFκB axis

Yi Li1, Ning Chen2, Chao Wu1

  • 1Department of Neurobiology, Capital Medical University, Beijing Center of Neural Regeneration and Repair, Key Laboratory for Neurodegenerative Diseases of the Ministry of Education, Beijing 100069, China.

Brain, Behavior, and Immunity
|November 1, 2019
PubMed

Insights

Galectin-1 therapy reduced microglia activation and protected dopamine neurons in Parkinson's disease models. This approach targets neuroinflammation and neuronal degeneration, offering a potential disease-modified treatment for Parkinson's disease.

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Parkinson's disease (PD) involves chronic microglia activation and dopamine neuron degeneration.
  • Targeting microglia activation is a promising strategy for PD therapy.

Purpose of the Study:

  • To evaluate galectin-1's therapeutic effects on microglia activation and neuronal degeneration in PD models.
  • To investigate galectin-1's mechanism of action in mitigating neuroinflammation.

Main Methods:

  • Galectin-1 was tested in lipopolysaccharide (LPS)-activated microglia and a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model.
  • Effects on cell apoptosis, motor deficits, dopaminergic neuron survival, and signaling pathways (MAPK, IκB/NFκB) were assessed.
  • The role of galectin-1's carbohydrate-recognition domain was examined using β-D-galactose.

Main Results:

  • Galectin-1 attenuated inflammatory insults and apoptosis in microglia-conditioned media.
  • Galectin-1 administration inhibited microglia activation, improved motor function, and preserved dopaminergic neurons in PD mice.
  • Galectin-1 dephosphorylated p38 and ERK1/2, inhibited IκB/NFκB signaling, and reduced pro-inflammatory cytokines (IL-1β, TNF-α) and inflammatory mediators (iNOS, COX-2).
  • These effects were blocked by β-D-galactose, indicating dependence on galectin-1's carbohydrate-recognition domain.

Conclusions:

  • Galectin-1 demonstrates significant neuroprotective effects in PD models.
  • Galectin-1 ameliorates neuroinflammation and dopaminergic neurodegeneration by modulating the MAPK/IκB/NFκB pathway via its carbohydrate-recognition domain.
  • Galectin-1 represents a potential therapeutic agent for Parkinson's disease.
Keywords:
Galectin-1Microglia activationNeuroinflammationParkinson’s disease

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