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Alaternin attenuates delayed neuronal cell death induced by transient cerebral hypoperfusion in mice.

Abstract
The aim of this study was to determine whether alaternin exhibits neuroprotective activity after transient cerebral hypoperfusion induced by bilateral common carotid artery occlusion (BCCAO). Mice were subjected to BCCAO, and circulation was restored after 20 min. Alaternin (10 mg/kg, p.o) treatment significantly prevented nitrotyrosine and lipid peroxidation, as well as BCCAO induced-inducible nitric oxide synthase (iNOS) expression. Alaternin also significantly reduced microglial activation (a marker of inflammation). The number of viable neurons detected by Nissl staining increased with alaternin (10 mg/kg, p.o) treatment at 7 days post-BCCAO. In the passive avoidance task, alaternin significantly ameliorated BCCAO-induced cognitive impairments (P<0.05). These results suggest that the neuroprotective effects of alaternin are mediated by its anti-inflammatory and radical scavenging activities.
AuthorsBum Young Shin, Dong Hyun Kim, Sook Kyung Hyun, Hyun Ah Jung, Jong Min Kim, Se Jin Park, Seong Yun Kim, Jae Hoon Cheong, Jae Sue Choi, Jong Hoon Ryu
JournalFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association (Food Chem Toxicol) Vol. 48 Issue 6 Pg. 1528-36 (Jun 2010) ISSN: 1873-6351 [Electronic] England
PMID20304026 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright 2010 Elsevier Ltd. All rights reserved.
Chemical References
  • 2-hydroxyemodin
  • Emodin
Topics
  • Animals
  • Avoidance Learning
  • Blotting, Western
  • Carotid Arteries (pathology)
  • Cell Death (drug effects)
  • Cerebrovascular Circulation
  • Emodin (analogs & derivatives, pharmacology)
  • Immunohistochemistry
  • Lipid Peroxidation
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neurons (drug effects)

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