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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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A Preclinical Model to Assess Brain Recovery After Acute Stroke in Rats
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Published on: November 6, 2019

Nicotinamide attenuates the ischemic brain injury-induced decrease of Akt activation and Bad phosphorylation.

Phil-Ok Koh1

  • 1Department of Anatomy, College of Veterinary Medicine and Research Institute of Life Science, Gyeongsang National University, 900 Gajwa-dong, Jinju, South Korea. pokoh@gnu.ac.kr

Neuroscience Letters
|May 21, 2011
PubMed
Summary
This summary is machine-generated.

Nicotinamide reduces brain damage from stroke by activating the Akt survival pathway. This vitamin B3 derivative enhances neuronal survival and protects against cerebral ischemic injury.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Cerebral ischemic injury, commonly known as stroke, leads to neuronal cell death.
  • Nicotinamide (vitamin B3) is known to activate cytoprotective mechanisms.
  • The Akt signaling pathway is crucial for neuronal survival.

Purpose of the Study:

  • To confirm the neuroprotective effects of nicotinamide in focal cerebral ischemic injury.
  • To investigate if nicotinamide modulates the Akt survival pathway and its downstream targets.
  • To elucidate the mechanism by which nicotinamide protects against stroke-induced brain damage.

Main Methods:

  • Adult male rats underwent middle cerebral artery occlusion (MCAO) to induce focal cerebral ischemia.
  • Animals were treated with either vehicle or nicotinamide (500 mg/kg) post-occlusion.
  • Infarct volume was measured, and protein levels (phosphorylated PDK1, Akt, Bad, and 14-3-3) were analyzed via Western blot.

Main Results:

  • Nicotinamide significantly reduced infarct volume in the cerebral cortex.
  • Nicotinamide treatment prevented the decrease in phosphorylated PDK1, Akt, and Bad levels caused by MCAO.
  • The interaction between phosphorylated Bad and 14-3-3, which is disrupted by MCAO, was maintained by nicotinamide.

Conclusions:

  • Nicotinamide demonstrates significant neuroprotective effects against focal cerebral ischemic injury.
  • These protective effects are mediated through the activation of the Akt signaling pathway.
  • Nicotinamide enhances neuronal survival by modulating the Akt pathway and its interaction with downstream targets like Bad.