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Isoflurane on brain inflammation.

Orhan Altay1, Hidenori Suzuki1, Yu Hasegawa1

  • 1Department of Physiology, Loma Linda University School of Medicine, Loma Linda, USA.

Neurobiology of Disease
|October 3, 2013
PubMed
Summary
This summary is machine-generated.

Subarachnoid hemorrhage (SAH) causes brain inflammation and injury. Isoflurane, an anesthetic, significantly reduced both SAH-induced brain injury and inflammation, possibly through the sphingosine pathway.

Keywords:
BWCBrain water contentCOX-2Cyclooxygenase-2DMSEBIEarly brain injuryICAM-1IL-1βInflammationIntercellular adhesion molecule-1Interleukin-1betaIonized calcium binding adaptor molecule-1IsofluraneMPOMyeloperoxidaseN, N-dimethylsphingosinePhosphorylated c-Jun N-terminal kinaseS1PS1P1/3SAHSphKSphingosine 1-phosphateSphingosine kinaseSphingosine-1-phosphate receptor-1/3Subarachnoid hemorrhageTNF-αTumor necrosis factor-alphaiba-1p-JNKvWFvon Willebrand factor

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Area of Science:

  • Neuroscience
  • Anesthesiology
  • Pathophysiology

Background:

  • Brain inflammation is a key factor in early brain injury following subarachnoid hemorrhage (SAH).
  • Understanding the mechanisms of SAH-induced neuroinflammation is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the development of brain inflammation after SAH.
  • To determine if the anesthetic isoflurane can prevent or mitigate brain inflammation and injury post-SAH.

Main Methods:

  • Subarachnoid hemorrhage was induced in mice via endovascular perforation.
  • Mice were treated with either vehicle or isoflurane, with subsequent analysis of brain injury markers and inflammatory mediators.
  • Specific inhibitors were used to explore the mechanism of isoflurane's effects, focusing on the sphingosine pathway.

Main Results:

  • SAH led to significant early brain injury and increased markers of inflammation, including inflammatory cells, cytokines, adhesion molecules, and inflammation inducers.
  • Isoflurane administration markedly reduced brain injury and suppressed the expression of key inflammatory markers.
  • The protective effects of isoflurane were diminished when sphingosine pathway inhibitors were administered.

Conclusions:

  • Isoflurane demonstrates significant neuroprotective effects against early brain injury following SAH.
  • Isoflurane effectively suppresses SAH-induced brain inflammation.
  • The findings suggest that isoflurane's beneficial actions may be mediated through the sphingosine-related signaling pathway.