Chronic ibuprofen treatment does not affect the secondary pathology in the thalamus or improve behavioral outcome in middle cerebral artery occlusion rats.

Anti-inflammatory drug ibuprofen decreases the β-amyloid (Aβ) deposition and associated inflammation in transgenic Alzheimer disease mice. Based on this, we studied whether ibuprofen could modulate the secondary pathology described in the thalamus of middle cerebral artery occlusion (MCAO) rats. Our hypothesis was that ibuprofen could decrease inflammatory reaction and Aβ load in the thalamus of MCAO rats, which in turn is reflected in improved behavioral outcome. Forty male Wistar rats (250-340 g) were subjected to sham-operation or transient occlusion of the right middle cerebral artery (120 min). Ibuprofen (4 0mg/kg/day, per os) was administrated for 27 days beginning the treatment on post-operative day 2. MCAO controls were given vehicle. Sensorimotor impairment was assessed using the limb-placing, tapered ledged beam-walking and cylinder tests during the follow-up. The rats were perfused for histology on postoperative day 29. Histological data showed that ibuprofen did not affect Aβ or calcium load in the thalamus of MCAO rats. In addition, behavioral tests did not show significant difference between vehicle- and ibuprofen-treated MCAO rats. The present data do not support the idea that ibuprofen reduces the secondary Aβ/calcium pathology in the thalamus or associated sensorimotor impairment following cerebral ischemia.