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Minocycline inhibits neuronal death and glial activation induced by beta-amyloid peptide in rat hippocampus.

Authors
Ryu, JK; Franciosi, S; Sattayaprasert, P; Kim, SU; McLarnon, JG
Citation
Glia, 48(1):85-90, 2004
Journal Title
Glia
ISSN
0894-14911098-1136
Abstract
Minocycline, a second-generation tetracycline compound, has been examined as a neuroprotectant in beta-amyloid (A beta)-injected rat hippocampus. At 7 days post-injection, A beta(1-42) caused a significant loss of granule cell layer neurons (28% reduction) compared to control uninjected hippocampus. Hippocampal injection of A beta peptide also led to marked gliosis with numbers of microglia (increased by 26-fold) and immunoreactivity of astrocytes (increased by 11-fold) relative to control, as determined from immunohistochemical analysis. Intraperitoneal administration of minocycline significantly reduced neuronal loss induced by A beta(1-42) (by 80%) and also diminished numbers of microglia (by 69%) and astrocytes (by 36%) relative to peptide alone. Peptide injection increased expression of cyclooxygenase-2 (COX-2) in most (about 70%) of granule cells, a subset (about 20%) of microglia, but not in astrocytes; in the presence of minocycline, COX-2 immunostaining was abolished in microglia. The results from this study suggest that minocycline may have efficacy in the treatment of AD.
MeSH terms
Amyloid beta-Peptides/*antagonists & inhibitors/pharmacologyAnimalsAnti-Bacterial Agents/*pharmacologyAnti-Inflammatory Agents, Non-SteroidalAstrocytes/drug effects/enzymologyCell Death/drug effectsCyclooxygenase 2GliosisHippocampus/*cytology/drug effectsImmunohistochemistryIsoenzymes/biosynthesisMaleMinocycline/*pharmacologyNerve Degeneration/pathologyNeuroglia/*drug effects/enzymologyNeurons/*drug effects/enzymology*Neuroprotective AgentsProstaglandin-Endoperoxide Synthases/biosynthesisRatsRats, Sprague-Dawley
DOI
10.1002/glia.20051
PMID
15326618
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
김, 승업
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