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Optimized Management of Endovascular Treatment for Acute Ischemic Stroke
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Microglia-Derived Adiposomes are Potential Targets for the Treatment of Ischemic Stroke

Chi-Hsin Lin1,2, Li-Ya Liao3, Tsung-Ying Yang4

  • 1Department of Medical Research, MacKay Memorial Hospital, New Taipei City, Taiwan.

Cellular and Molecular Neurobiology
|March 11, 2019
PubMed

Insights

Adiposomes worsen brain inflammation and cell death after cerebral ischemia. Inhibiting adiposome formation or PPARγ reduces inflammation and brain damage, suggesting new stroke treatment targets.

Area of Science:

  • Neuroscience
  • Inflammation Research
  • Stroke Pathophysiology

Background:

  • Cerebral ischemia triggers brain inflammation.
  • Adiposomes are implicated as depots for inflammatory mediators.
  • The role of adiposomes in ischemic microglia and brain tissue requires further investigation.

Purpose of the Study:

  • To investigate the pro-inflammatory and pro-death roles of adiposomes in ischemic microglia and brain.
  • To evaluate the contribution of PPARγ to adiposome formation in ischemic microglia.

Main Methods:

  • Utilized focal cerebral ischemia/reperfusion (I/R) animal model and in vitro glucose-oxygen-serum deprivation (GOSD) cell model.
  • Assessed adiposome formation, inflammatory activity, microglia cell death, and brain infarction.
  • Administered adiposome inhibitor (NS-398) and PPARγ antagonist (GW9662) to evaluate their effects.

Main Results:

  • GOSD-induced adiposome formation significantly increased microglial inflammatory activity (TNF-α, IL-1β) and cell death.
  • PPARγ partially contributed to adiposome formation and microglial inflammatory responses.
  • Inhibition of adiposome formation (NS-398) or PPARγ (GW9662) reduced microglial inflammation, cell death, brain infarct volume, and motor deficits in ischemic rats.

Conclusions:

  • Microglia-derived adiposomes play a pathological role in cerebral ischemia through pro-inflammatory and pro-death effects.
  • Adiposomes and their regulator PPARγ represent potential therapeutic targets for ischemic stroke.
  • NS-398 and GW9662 show potential therapeutic value in treating ischemic stroke.
Keywords:
AdiposomeCerebral ischemiaInflammationMicrogliaPPARγ

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