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Related Experiment Video

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Assessing Retinal Microglial Phagocytic Function In Vivo Using a Flow Cytometry-based Assay

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Published on: October 18, 2016

Modulation of microglial functions by methyl jasmonate.

Jordan A McKenzie¹, Andis Klegeris¹

¹Biology Department, University of British Columbia Okanagan Campus, Kelowna, BC, Canada.

Neural Regeneration Research

|July 21, 2018

Summary

Methyl jasmonate (MJ) shows potential for Alzheimer's disease (AD) treatment by reducing harmful inflammation. This compound was found to decrease damaging reactive oxygen species and enhance microglial phagocytosis, aiding in the clearance of amyloid aggregates.

Keywords:

Alzheimer's disease anti-inflammatory glia neurodegeneration neuroinflammation neuroprotection nitric oxide phagocytosis reactive nitrogen species reactive oxygen species

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Last Updated: Feb 7, 2026

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Published on: October 5, 2014

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Published on: January 2, 2009

Area of Science:

Neuroscience
Pharmacology
Immunology

Background:

Neuroinflammation, orchestrated by microglial cells, is a key factor in Alzheimer's disease (AD) pathogenesis.
Methyl jasmonate (MJ) exhibits anti-inflammatory properties in peripheral models and has shown recent anti-neuroinflammatory effects in vivo.
The precise mechanisms underlying MJ's neuroprotective effects remain largely uncharacterized.

Purpose of the Study:

To investigate the effects of Methyl Jasmonate (MJ) on key microglial cell functions.
To elucidate the cellular and molecular mechanisms of MJ's anti-neuroinflammatory activity.
To evaluate MJ as a potential therapeutic agent for Alzheimer's disease.

Main Methods:

Utilized two distinct in vitro microglial models: human HL-60 promyelocytic leukemia cells and murine BV-2 microglia.
Assessed the impact of MJ on reactive oxygen species (ROS) production and cell viability.
Quantified changes in microglial phagocytic activity and nitric oxide (NO) secretion following MJ treatment.

Main Results:

Methyl jasmonate (MJ) significantly inhibited the production of reactive oxygen species (ROS) in HL-60 cells without affecting cell viability.
MJ selectively upregulated the phagocytic capacity of BV-2 microglial cells.
No significant effect of MJ was observed on nitric oxide (NO) secretion by BV-2 microglia.

Conclusions:

Methyl jasmonate (MJ) demonstrates a dual action on microglia: reducing oxidative stress and enhancing phagocytosis.
The observed effects suggest MJ's potential to facilitate the clearance of amyloid-beta aggregates, a hallmark of AD.
These findings support further investigation of MJ as a therapeutic candidate for managing neuroinflammation in Alzheimer's disease.