<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Michel-Monigadon D</dc:creator>
  <dc:creator>Bonny C</dc:creator>
  <dc:creator>Hirt L</dc:creator>
  <dc:date>2010</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">BACKGROUND
Inhibition of the c-Jun N-terminal kinase (JNK) pathway by the TAT-coupled peptide XG-102 (formerly D- JNKI1) induces strong neuroprotection in ischemic stroke in rodents. We investigated the effect of JNK inhibition in intracerebral hemorrhage (ICH).


METHODS
Three hours after induction of ICH by intrastriatal collagenase injection in mice, the animals received an intravenous injection of 100 microg/kg of XG-102. The neurological outcome was assessed daily and the mice were sacrificed at 6 h, 1, 2 or 5 days after ICH.


RESULTS
XG-102 administration significantly improved the neurological outcome at 1 day (p &lt; 0.01). The lesion volume was significantly decreased after 2 days (29 +/- 11 vs. 39 +/- 5 mm(3) in vehicle-treated animals, p &lt; 0.05). There was also a decreased hemispheric swelling (14 +/- 13 vs. 26 +/- 9% in vehicle-treated animals, p &lt; 0.05) correlating with increased aquaporin 4 expression.


CONCLUSIONS
XG-102 attenuates cerebral edema in ICH and functional impairment at early time points. The beneficial effects observed with XG-102 in ICH, as well as in ischemic stroke, open the possibility to rapidly treat stroke patients before imaging, thereby saving precious time.</dc:description>
  <dc:identifier>https://sonar.ch/global/documents/78374</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1159/000306643</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/20375499</dc:relation>
  <dc:source>Cerebrovascular diseases (Basel, Switzerland). - 2010</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Animals</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Aquaporin 4</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Behavior, Animal</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Brain</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Brain Edema</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Brain Ischemia</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Cerebral Hemorrhage</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Collagenases</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">Enzyme Activation</dc:subject>
  <dc:subject xmlns:ns10="xml" ns10:lang="en">Immunohistochemistry</dc:subject>
  <dc:subject xmlns:ns11="xml" ns11:lang="en">JNK Mitogen-Activated Protein Kinases</dc:subject>
  <dc:subject xmlns:ns12="xml" ns12:lang="en">Macrophage Activation</dc:subject>
  <dc:subject xmlns:ns13="xml" ns13:lang="en">Mice</dc:subject>
  <dc:subject xmlns:ns14="xml" ns14:lang="en">Mice, Inbred ICR</dc:subject>
  <dc:subject xmlns:ns15="xml" ns15:lang="en">Neuroglia</dc:subject>
  <dc:subject xmlns:ns16="xml" ns16:lang="en">Peptides</dc:subject>
  <dc:subject xmlns:ns17="xml" ns17:lang="en">Postural Balance</dc:subject>
  <dc:subject xmlns:ns18="xml" ns18:lang="en">Protein Kinase Inhibitors</dc:subject>
  <dc:subject xmlns:ns19="xml" ns19:lang="en">Treatment Outcome</dc:subject>
  <dc:title xmlns:ns20="xml" ns20:lang="en">c-Jun N-terminal kinase pathway inhibition in intracerebral hemorrhage.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>