EFFECT OF α-TOCOTRIENOL AND PROXISOME PROLIFRATIVE-ACTIVATED RECEPTOR LIGAND ON THE BRAIN ISCHEMIA IN MALE RAT

BACKGROUND AND OBJECTIVE: Stroke is one of the leading causes of death and disability in the world. Previous studies have demonstrated that α-tocotrienol (α-TCT) and rosiglitazone (RGZ) reduce ischemic damage by middle cerebral artery (MCA) occlusion when administered before ischemic stroke in mice...

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Autores principales: MA Allahtavakoli, A Shamsizadeh, M Mahmoodi, R Moloudi, ME Rezvani
Formato: article
Lenguaje:EN
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Publicado: Babol University of Medical Sciences 2008
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Acceso en línea:https://doaj.org/article/49a63bd667664ece8c48bf56eb084b0e
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Sumario:BACKGROUND AND OBJECTIVE: Stroke is one of the leading causes of death and disability in the world. Previous studies have demonstrated that α-tocotrienol (α-TCT) and rosiglitazone (RGZ) reduce ischemic damage by middle cerebral artery (MCA) occlusion when administered before ischemic stroke in mice and rats. The aim of this study was to investigate the neuroprotective effects of α-TCT and RGZ at 3 hours after cerebral ischemia. METHODS: In this experimental study, stroke was induced by embolizing a preformed clot into the MCA. Male Wistar rats (300-350 gr) were assigned to α-TCT (1 or 10 mg/kg), rosiglitazone (RGZ) and sham-operation. The drugs were injected i.p. Stained brain sections were scanned and infarct area were determined using a picture analyzer software. FINDINGS: Forty eight hours after embolic ischemia, infarct volume in the control, RGZ, low and high doses of α-TCT were 29.4±2.6%, 15.9±3.1%, 24.9±2.1% and 29±4.8%, respectively. There was a significant difference between control and RGZ groups (p<0.05). Compared to the control group, the low and high doses of α-TCT didn’t show any significant difference. Furthermore, only RGZ decreased neurological deficits (p<0.05) and sensory impairments (p<0.01). CONCLUSION: Administration of α-TCT at 3 hr after induction of cerebral ischemia is not neuroprotective but RGZ may have beneficial effects on treatment and management of stroke. So further studies are needed to survey the neuroprotective effects of α-TCT after stroke.