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      Protective role of luteolin against cognitive dysfunction induced by chronic cerebral hypoperfusion in rats.

      Pharmacology, Biochemistry, and Behavior
      Amyloid Precursor Protein Secretases, metabolism, Amyloid beta-Peptides, drug effects, Animals, Aspartic Acid Endopeptidases, Brain Ischemia, complications, drug therapy, Cerebral Cortex, blood supply, Cognition Disorders, etiology, Dose-Response Relationship, Drug, Free Radical Scavengers, pharmacology, therapeutic use, Hippocampus, Inflammation Mediators, Interleukin-1beta, Luteolin, Male, Maze Learning, NF-kappa B, Neuroprotective Agents, Peptide Fragments, Rats, Tumor Necrosis Factor-alpha

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          Abstract

          Chronic cerebral hypoperfusion, a mild ischemic condition, is associated with the cognitive deficits of Alzheimer's disease (AD). Luteolin, a polyphenolic compound found in foods of plant origin, belonging to the flavone subclass of flavonoids, has been shown to possess antioxidant, anti-inflammatory and antitumorigenic properties. In the present study, the effects of luteolin on chronic cerebral hypoperfusion-associated neurocognitive pathologies were investigated by using rats with permanent bilateral common carotid artery occlusion, a rat model of chronic cerebral hypoperfusion. As expected, we found that luteolin could attenuate cognitive dysfunction in chronic cerebral hypoperfused rats, as assessed using Morris water maze tests. Daily oral administration of luteolin (50, 100 and 200mg/kg) significantly scavenged oxygen free radicals, enhanced antioxidant potential, decreased the lipid peroxide production and suppressed inflammatory reaction in the cerebral cortex and hippocampus induced by chronic cerebral hypoperfusion. Meanwhile, the results indicated that cerebral hypoperfusion activated nuclear factor-κB (NF-κB), increased the expression of β-site amyloid precursor protein cleaving enzyme (BACE1), as well as elevated amyloid beta (Aβ) levels in the cortex and hippocampus. However, long-term administration of luteolin significantly down-regulated the expression of NF-κB and BACE1, accompanied by diminishing the deposition of Aβ. Our results suggest a potential therapeutic use of luteolin for cerebral hypoperfusion associated cognitive dysfunction in AD. Copyright © 2014 Elsevier Inc. All rights reserved.

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