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Intrastriatal Injection of Autologous Blood or Clostridial Collagenase as Murine Models of Intracerebral Hemorrhage
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c-Jun N-terminal kinase pathway inhibition in intracerebral hemorrhage

Delphine Michel-Monigadon1, Christophe Bonny, Lorenz Hirt

  • 1Department of Clinical Neuroscience, Neurology Service, Centre Hospitalier Universitaire Vaudois and Lausanne University, Lausanne, Switzerland.

Cerebrovascular Diseases (Basel, Switzerland)
|April 9, 2010
PubMed

Insights

The JNK inhibitor XG-102 reduced brain swelling and improved neurological function in mice with intracerebral hemorrhage (ICH). This suggests XG-102 could be a rapid treatment for stroke patients.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cerebrovascular Disease Research

Background:

  • The c-Jun N-terminal kinase (JNK) pathway is implicated in brain injury.
  • JNK inhibition with XG-102 shows neuroprotection in ischemic stroke models.
  • The efficacy of JNK inhibition in intracerebral hemorrhage (ICH) requires investigation.

Purpose of the Study:

  • To investigate the therapeutic effect of JNK inhibition by XG-102 in a mouse model of intracerebral hemorrhage (ICH).

Main Methods:

  • Intracerebral hemorrhage (ICH) was induced in mice via collagenase injection.
  • Animals received intravenous injections of XG-102 (100 microg/kg) three hours post-ICH.
  • Neurological outcomes were assessed daily, with sacrifice at 6 hours, 1, 2, or 5 days post-ICH.

Main Results:

  • XG-102 significantly improved neurological outcomes by day 1 (p < 0.01).
  • Lesion volume decreased by day 2 (29 +/- 11 vs. 39 +/- 5 mm(3); p < 0.05).
  • Hemispheric swelling was reduced (14 +/- 13 vs. 26 +/- 9%; p < 0.05), correlating with increased aquaporin 4 expression.

Conclusions:

  • XG-102 attenuates cerebral edema and functional deficits in early stages of ICH.
  • Beneficial effects in ICH, similar to ischemic stroke, suggest potential for rapid pre-imaging treatment in stroke patients.
Abstract

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