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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...

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Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents
07:52

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Published on: June 2, 2015

Brain ischemic preconditioning does not require PARP-1.

Giuseppe Faraco1, Francesco Blasi, Wookee Min

  • 1Department of Pharmacology, University of Florence, Italy.

Stroke
|November 7, 2009
PubMed
Summary

Poly(ADP-ribose) polymerase-1 (PARP-1) is not essential for brain ischemic preconditioning in mice. Studies show PARP-1 inhibition or knockout did not affect the protective effects of preconditioning.

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Area of Science:

  • Neuroscience
  • Cardiovascular Research
  • Biochemistry

Background:

  • Poly(ADP-ribose) polymerase-1 (PARP-1) is implicated in ischemic preconditioning in cardiac and neuronal cells.
  • The role of PARP-1 in brain ischemic preconditioning remains unelucidated.

Purpose of the Study:

  • To investigate the involvement of PARP-1 in brain ischemic preconditioning.
  • To determine if pharmacological inhibition or genetic knockout of PARP-1 affects ischemic protection in the brain.

Main Methods:

  • Mouse model utilizing bilateral common carotid artery occlusion (BCCAO) for preconditioning.
  • Middle cerebral artery occlusion (MCAO) was used to induce stroke 24 hours after BCCAO.
  • Pharmacological inhibition of PARP-1 and use of PARP-1 knockout (KO) mice.

Main Results:

  • A 5-minute BCCAO significantly reduced infarct volumes 24 hours later following MCAO.
  • Pharmacological PARP-1 inhibition between BCCAO and MCAO did not abolish the preconditioning effect.
  • Levels of PARP-1 substrate (NAD), product (poly(ADP-ribose)), caspase-3 activation, and PARP-1 expression remained unchanged post-BCCAO.
  • PARP-1 KO mice exhibited similar protection from preconditioning as wild-type mice.

Conclusions:

  • PARP-1 is dispensable for brain ischemic preconditioning.
  • These findings contrast with the known role of PARP-1 in cardiac ischemic preconditioning.