Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5854174 | Food and Chemical Toxicology | 2010 | 9 Pages |
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 20Â min. Alaternin (10Â 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 (10Â mg/kg, p.o) treatment at 7Â days post-BCCAO. In the passive avoidance task, alaternin significantly ameliorated BCCAO-induced cognitive impairments (PÂ <Â 0.05). These results suggest that the neuroprotective effects of alaternin are mediated by its anti-inflammatory and radical scavenging activities.
Keywords
PMSFNOSTBARSiNOSEGTAGFAPPVDFTTBSBCCAoPBSABCROSEDTAethylene glycol tetraacetic acidEthylenediaminetetraacetic acidanalysis of varianceANOVAMemorybilateral common carotid artery occlusioninducible nitric oxide synthasephenylmethylsulphonyl fluoridePhosphate-buffered salinethiobarbituric acid reactive substancesMicroglianitrotyrosineNitric oxidenitric oxide synthaseCoeGlial fibrillary acidic proteinPolyvinylidene fluorideReactive oxygen species
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Authors
Bum 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,