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Updated: May 6, 2026
Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
Published on: February 12, 2016
M2 macrophage-derived exosomes mitigate acute inflammation following ischemic stroke
Jinyang Song1, Gang Su2, Wei Chen1
1The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, Gansu, China.
Background:
The acute inflammatory response following ischemic stroke is a key factor in exacerbating brain injury. Modulating excessive inflammation during the oxidative stress (OS) phase represents a potential therapeutic strategy; however, clinical interventions remain limited.
Methods:
M0 and M2 macrophage-derived exosomes (M0-exo and M2-exo) were administered to microglia under oxygen-glucose deprivation/reperfusion (OGD/R) conditions and to mice subjected to transient middle cerebral artery occlusion (tMCAO). The mechanisms underlying their anti-inflammatory effects were then investigated through a combination of bioinformatic analysis and fundamental experiments.
Results:
Treatment with exosomes markedly suppressed the expression of pro-inflammatory factors. Furthermore, they significantly reduced cerebral infarct volume and improved neurological function in mice. Notably, the anti-inflammatory effect of M2-exo was significantly superior to that of M0-exo. miRNA sequencing and subsequent validation revealed a specific enrichment of miR-330-5p in M2-exo. Mechanistic studies have demonstrated that miR-330-5p suppresses the expression of Spleen tyrosine kinase (Syk) and signal transducer and activator of transcription 3 (Stat3) in microglia, consequently reducing the production of downstream inflammatory factors. Treatment with Syk or Stat3 inhibitors partially mimicked the anti-inflammatory action of miR-330-5p in rescue studies.
Conclusion:
Our results unveil a novel anti-inflammatory pathway mediated by M2-exo, providing novel insights for stroke therapy.
