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A Preclinical Model to Assess Brain Recovery After Acute Stroke in Rats

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Nicotinamide attenuates the decrease of astrocytic phosphoprotein PEA-15 in focal cerebral ischemic injury.

¹Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, Jinju 660–701, South Korea. pokoh@gnu.ac.kr

The Journal of Veterinary Medical Science

|November 10, 2011

Summary

Nicotinamide protects the brain from stroke injury by maintaining levels of the anti-apoptotic protein Phosphoprotein enriched in astrocytes 15 (PEA-15) and its phosphorylated forms. This neuroprotective effect involves preventing cell death pathways.

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Area of Science:

Neuroscience
Biochemistry
Cell Biology

Background:

Focal cerebral ischemic injury, such as stroke, leads to significant neuronal damage and cell death.
Phosphoprotein enriched in astrocytes 15 (PEA-15) is a key anti-apoptotic protein found in astrocytes.
Astrocytic PEA-15 plays a crucial role in protecting neurons from apoptotic cell death.

Purpose of the Study:

To investigate the effect of nicotinamide on PEA-15 and its phosphorylated forms (Serine 104 and 116) in a rat model of ischemic stroke.
To determine if nicotinamide modulates PEA-15 expression and phosphorylation following middle cerebral artery occlusion (MCAO).

Main Methods:

Adult male rats underwent MCAO to induce ischemic injury.
Rats were treated with either vehicle or nicotinamide (500 mg/kg) 2 hours post-MCAO.
Cerebral cortices were collected 24 hours after MCAO for proteomic and Western blot analyses.

Main Results:

MCAO induced a significant decrease in PEA-15 protein levels.
Nicotinamide treatment attenuated the MCAO-induced reduction in PEA-15 levels.
Western blot analysis revealed that nicotinamide prevented the injury-induced decrease in phospho-PEA-15 (Serine 104 and Serine 116) levels.

Conclusions:

Nicotinamide exerts neuroprotective effects against focal cerebral ischemic injury.
The neuroprotection is mediated, in part, by the preservation of PEA-15 and its phosphorylated forms, which are critical for anti-apoptotic functions.
Nicotinamide may represent a therapeutic strategy for stroke by preventing MCAO-induced decreases in PEA-15 and its phosphorylation.