Neuroprotective Efficacy of the Peroxisome Proliferator-Activated Receptor-gamma Ligand in Chronic Cerebral Hypoperfusion

SAYAN ÖZAÇMAK H., SAYAN H., BARUT F., Jakubowska-Dogru E.

CURRENT NEUROVASCULAR RESEARCH, vol.8, no.3, pp.190-199, 2011 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 8 Issue: 3
  • Publication Date: 2011
  • Doi Number: 10.2174/156720211796558087
  • Journal Name: CURRENT NEUROVASCULAR RESEARCH
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.190-199
  • Keywords: Chronic cerebral hypoperfusion, S100, synaptophysin, spatial learning, ISCHEMIC BRAIN-INJURY, WHITE-MATTER DAMAGE, PPAR-GAMMA, OXIDATIVE STRESS, COGNITIVE IMPAIRMENT, MEMORY IMPAIRMENT, RAT MODEL, ALZHEIMERS-DISEASE, NEURONAL DAMAGE, MOUSE MODEL
  • Middle East Technical University Affiliated: Yes

Abstract

Chronic cerebral hypoperfusion can cause learning and memory impairment and neuronal damage resembling the effects observed in vascular dementia. PPAR-gamma agonists were shown to modulate inflammatory response and neuronal death following cerebral ischemia. The present study was designed to evaluate possible neuroprotective effects of rosiglitazone, a PPAR-gamma agonist, in rat model of chronic cerebral hypoperfusion. Cerebral hypoperfusion was induced by permanent bilateral occlusion of the common carotid arteries. Oral administration of rosiglitazone (1.5, 3, and 6 mg/kg/day) or vehicle was carried out for 5 weeks, starting one week before the surgery. Cognitive performance was assessed using the Morris water maze. The density of S100B protein-immunoreactive astrocytes and the OX-42-labeled microglial activation were estimated. Synaptogenesis was also evaluated by the measurement of synaptophysin, the pre-synaptic vesicular protein, level via western blotting technique.