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Auraptene Acts as an Anti-Inflammatory Agent in the Mouse Brain
Satoshi Okuyama1, Mayu Morita2, Miki Kaji3
1Department of Pharmaceutical Pharmacology, College of Pharmaceutical Sciences, Matsuyama University, 4-2 Bunkyo-cho, Matsuyama, Ehime 790-8578, Japan. sokuyama@cc.matsuyama-u.ac.jp.
Molecules (Basel, Switzerland)
|November 17, 2015
Summary
Auraptene (AUR), a citrus coumarin, reduces brain inflammation and neuronal damage after ischemic stroke. Pretreatment with AUR suppresses microglial activation and inflammatory gene expression in brain cells.
Area of Science:
- Neuroscience
- Pharmacology
- Inflammation Research
Background:
- Auraptene (AUR), a citrus coumarin, is known for its anti-inflammatory properties in peripheral tissues.
- Previous studies demonstrated AUR's anti-inflammatory effects in the ischemic brain, potentially mediated by astrocyte-derived inflammatory mediators.
Purpose of the Study:
- To investigate the direct anti-inflammatory effects of auraptene (AUR) on the ischemic brain.
- To determine AUR's impact on microglial activation and inflammatory mediator expression in astrocytes.
Main Methods:
- Mice were pretreated with AUR before and after ischemic surgery.
- AUR's effects on microglial activation, cyclooxygenase-2 (COX-2) expression, and COX-2 mRNA in the hippocampus were assessed.
- The impact of AUR on lipopolysaccharide-induced inflammatory gene expression in cultured astrocytes was evaluated.
- AUR levels in the brain were measured after intraperitoneal administration.
Main Results:
- AUR pretreatment suppressed microglial activation and COX-2 expression in astrocytes within the hippocampus.
- AUR significantly reduced COX-2 mRNA expression in the hippocampus.
- In cultured astrocytes, AUR suppressed lipopolysaccharide-induced expression of COX-2 mRNA and pro-inflammatory cytokines.
- AUR was detected in the brain within 60 minutes of administration.
Conclusions:
- Auraptene (AUR) exerts direct anti-inflammatory effects within the brain.
- AUR pretreatment offers neuroprotection by suppressing key inflammatory pathways in astrocytes and microglia following ischemic events.

