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(Stroke. 2007;38:381.)
© 2007 American Heart Association, Inc.

Original Contributions

Effects of Triflusal and Aspirin in a Rat Model of Cerebral Ischemia

Shawn N. Whitehead, PhD; Nestor A. Bayona, MSc; Guanliang Cheng, MD; Gary V. Allen, PhD; Vladimir C. Hachinski, MD David F. Cechetto, PhD

From Department of Anatomy and Cell Biology (S.N.W., N.A.B., G.C., D.F.C.), University of Western Ontario, London, Canada; Department of Anatomy & Neurobiology (G.V.A.), Faculty of Medicine, Sir Charles Tupper Medical Building, Dalhousie University, Halifax, Nova Scotia; Faculty of Medicine and Dentistry (V.C.H.), University of Western Ontario, London, Canada.

Correspondence to David F. Cechetto, Department of Anatomy and Cell Biology, University of Western Ontario, London, Canada N6A 5C1. E-mail cechetto{at}uwo.ca

Background and Purpose— Neuroinflammation plays a critical role in the pathogenesis of cerebral ischemia. Triflusal, a selective cyclooxygenase-2, and its active metabolite 3-hydroxy-4-trifluoromethylbenzoic acid may inhibit apoptosis and inflammation after cerebral ischemia. An in vivo model of cerebral ischemia was used to investigate the effects of triflusal and aspirin treatment on infarct volume, and inflammation after cerebral ischemia in the rat.

Methods— Male Wistar rats were subjected to a permanent right-sided middle cerebral artery occlusion. Rats received oral administration of either triflusal or aspirin. After 3 days after surgery, immunostaining was used to detect neuroinflammatory cells and molecules, and infarct volumes were measured.

Results— Both triflusal and aspirin at a dose of 30 mg/kg but not 10 mg/kg significantly reduced infarct volume compared with vehicle treatment. Middle cerebral artery occlusion resulted in increased astrocyte and heat shock protein-27 (Hsp27) immunostaining in the ipsilateral cortex. Triflusal (30 mg/kg) or aspirin treatment (30 mg/kg) did not reduce the levels of GFAP or Hsp27 immunostaining. Triflusal (30 mg/kg) also significantly decreased the protein levels of IL-Iß but not nuclear factor kappa B or tumor necrosis factor- in the cortex ipsilateral to the middle cerebral artery occlusion.

Conclusions— The results suggest that triflusal and aspirin appear to be equally neuroprotective against middle cerebral artery occlusion-induced cerebral ischemia. Therefore, strong rationale exists to continue the neuroprotective examination of triflusal in brain injury.

Key Words: astrocytes • cerebral ischemia • cytokines • inflammation • reactive microglia