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Inhibitory effect with antisense mitogen-activated protein kinase oligodeoxynucleotide against cerebral vasospasm in

Motoyoshi Satoh1, Andrew D Parent, John H Zhang

  • 1Department of Neurosurgery, University of Mississippi Medical Center, Jackson, Miss 39216, USA.

Stroke
|March 2, 2002
PubMed
Abstract

Insights

Mitogen-activated protein kinase (MAPK) activation, not expression, is linked to cerebral vasospasm after subarachnoid hemorrhage (SAH). Antisense MAPK oligodeoxynucleotide (ODN) effectively treats this condition.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Cerebral vasospasm following subarachnoid hemorrhage (SAH) is a critical complication.
  • Mitogen-activated protein kinase (MAPK) pathways are implicated in vascular smooth muscle contraction.

Purpose of the Study:

  • To investigate the role of MAPK expression and activation in the pathogenesis of cerebral vasospasm post-SAH.
  • To evaluate the therapeutic potential of antisense MAPK oligodeoxynucleotide (ODN) for treating cerebral vasospasm.

Main Methods:

  • Utilized a rat model of experimental subarachnoid hemorrhage (SAH).
  • Administered antisense MAPK, sense MAPK, or scrambled oligodeoxynucleotides (ODNs) intracisternally.
  • Assessed basilar artery vasospasm using histological parameters and quantified MAPK expression/activation via immunohistochemistry and Western blot.

Main Results:

  • Antisense MAPK ODN significantly inhibited cerebral vasospasm compared to control ODNs on day 2 post-SAH.
  • Immunohistochemistry and Western blot confirmed inhibition of MAPK and phosphorylated MAPK in the basilar artery.
  • Post-SAH treatment with antisense ODN attenuated both MAPK activation and cerebral vasospasm.

Conclusions:

  • MAPK activation, rather than expression, appears to be crucial for sustained smooth muscle contraction in cerebral vasospasm after SAH.
  • Antisense MAPK ODN presents a promising therapeutic strategy for managing cerebral vasospasm.

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