Volume 7 Supplement 1

International Society on Brain and Behaviour: 3rd International Congress on Brain and Behaviour

Open Access

Effect of Rosiglitazone, on infarct volume and neurological deficits in local brain ischaemia

  • Mohammad Allahtavakoli1 and
  • Aliasghar Pourshanazari
Annals of General Psychiatry20087(Suppl 1):S358

DOI: 10.1186/1744-859X-7-S1-S358

Published: 17 April 2008

Background

Stroke is accompanied by a robust inflammatory response, glutamate-mediated excitotoxicity, release of reactive oxygen species and apoptosis. Thiazolidinediones, which target the nuclear receptor peroxisome proliferator-activated receptor (PPAR)-g, have been reported recently to exhibit potent anti-inflammatory and anti-oxidant actions and inhibit both neural excitotoxicity and apoptosis.

Materials and methods

The present study was conducted to determine whether rosiglitazone, a potent thiazolidinedione for PPAR-g, would show efficacy against the cerebral infarction and neurological dysfunctions induced by embolic middle cerebral artery (MCA) occlusion in the rat. Focal ischaemic injury was induced by embolizing a preformed clot into the MCA. Rosiglitazone was dissolved in dimethyl sulphoxide and injected i.p. 1 h before MCA occlusion at doses of 0.033, 0.1, 0.3 or 1 mg/kg. Forty-eight hours after MCA occlusion, brains were removed, sectioned and stained with a 2% solution of 2,3,5-triphenyltetrazolum chloride and analysed using a commercial image-processing software program.

Results

When rosiglitazone was administered 1 h before embolization, it significantly reduced infarct volume by 48.2, 68.4% and 70.3% at doses of 0.1, 0.3 and 1 mg/kg, respectively (P < 0.001). Rosiglitazone-treated rats also demonstrated improved neurological functions. However, there were no statistically significant differences between control and treated groups in terms of brain oedema at 48 h after ischaemic injury.

Conclusions

The findings of the present study may support the idea of a potential benefit of thiazolidinediones in the management of ischaemic stroke.

Declarations

Acknowledgements

This research supported by Tehran university grants.

Authors’ Affiliations

(1)
Physiology Dept., Medical School, Rafsanjan University of Medical Sciences

Copyright

© Allahtavakoli and Pourshanazari; licensee BioMed Central Ltd. 2008

This article is published under license to BioMed Central Ltd.

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