Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Prior ischemic stress protects against experimental stroke

R P Simon1, M Niiro, R Gwinn

  • 1Department of Neurology, University of California, San Francisco Medical Center 94143-0870.

Neuroscience Letters
|December 12, 1993
PubMed
Summary

Prior ischemic stress in rats protected against brain damage by inducing neuronal stress and heat shock protein 72 (HSP72). This preconditioning reduced the severity of subsequent cerebral infarction, suggesting a protective mechanism against stroke injury.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Corrigendum to "Expression of the proto-oncogene bcl-2 is increased in the rat brain following kainate-induced seizures" [Restor. Neurol. Neurosci. 9 (1996) 243].

Restorative neurology and neuroscience·2011
Same author

Expression of the proto-oncogene bcl-2 is increased in the rat brain following kainate-induced seizures.

Restorative neurology and neuroscience·2011
Same author

Epileptic sudden death: animal models.

Epilepsia·2009
Same author

Contrasting patterns of Bim induction and neuroprotection in Bim-deficient mice between hippocampus and neocortex after status epilepticus.

Cell death and differentiation·2009
Same author

Microarray profile of seizure damage-refractory hippocampal CA3 in a mouse model of epileptic preconditioning.

Neuroscience·2007
Same author

Ca2+ -permeable acid-sensing ion channels and ischemic brain injury.

The Journal of membrane biology·2006

Area of Science:

  • Neuroscience
  • Pathophysiology
  • Molecular Biology

Background:

  • Cerebral infarction, a major cause of stroke, results in significant neuronal damage.
  • The potential for preconditioning to mitigate ischemic injury is an area of active research.
  • Heat shock proteins (HSPs) are known cellular protectants.

Purpose of the Study:

  • To investigate the role of prior ischemic stress as a protective mechanism against cerebral infarction.
  • To determine if prior global cerebral ischemia influences the outcome of subsequent focal cerebral ischemia.
  • To examine the association between neuronal stress, heat shock protein 72 (HSP72) induction, and protection from ischemic injury.

Main Methods:

  • Rats were subjected to two brief periods of global cerebral ischemia separated by 24 hours.

Related Experiment Videos

  • Neuronal stress was assessed by measuring the induction of heat shock protein 72 (HSP72).
  • Focal cerebral ischemia was induced via permanent middle cerebral artery occlusion 48 hours after the initial ischemic stress.
  • Infarct volume was compared between preconditioned animals and sham-operated controls.

    • Main Results:

    • Prior global cerebral ischemia did not induce cell death but caused significant neuronal stress, evidenced by HSP72 induction.
    • Animals subjected to prior ischemic stress exhibited significantly smaller infarct volumes following permanent middle cerebral artery occlusion compared to controls.
    • A clear association was observed between ischemia-induced stress, HSP72 upregulation, and reduced brain injury.

    Conclusions:

    • Prior ischemic stress acts as a preconditioning stimulus, conferring protection against subsequent cerebral infarction.
    • The induction of heat shock protein 72 (HSP72) is a key component of the protective response to ischemic stress.
    • These findings highlight a potential therapeutic strategy involving preconditioning to attenuate stroke-related brain damage.