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Inhibition of thrombin-induced microglial activation and NADPH oxidase by minocycline protects dopaminergic neurons in the substantia nigra in vivo.

Authors
Choi, SH; Lee, DY; Chung, ES; Hong, YB; Kim, SU; Jin, BK
Citation
Journal of neurochemistry, 95(6):1755-1765, 2005
Journal Title
Journal of neurochemistry
ISSN
0022-30421471-4159
Abstract
The present study shows that activation of microglial NADPH oxidase and production of reactive oxygen species (ROS) is associated with thrombin-induced degeneration of nigral dopaminergic neurons in vivo. Seven days after thrombin injection in the rat substantia nigra (SN), tyrosine hydroxylase immunocytochemistry showed a significant loss of nigral dopaminergic neurons. This cell death was accompanied by localization of terminal deoxynucleotidyl transferase-mediated fluorecein UTP nick-end labelling (TUNEL) staining within dopaminergic neurons. This neurotoxicity was antagonized by the semisynthetic tetracycline derivative, minocycline, and the observed neuroprotective effects were associated with the ability of minocycline to suppress NADPH oxidase-derived ROS production and pro-inflammatory cytokine expression, including interleukin-1beta and inducible nitric oxide synthase, from activated microglia. These results suggest that microglial NADPH oxidase may be a viable target for neuroprotection against oxidative damage.
MeSH terms
AnimalsAnti-Bacterial Agents/pharmacology*Blotting, WesternDopamine/physiology*Enzyme Inhibitors*FemaleFluorescent Antibody TechniqueImmunohistochemistryIn Situ Nick-End LabelingInterleukin-1/biosynthesisMacrophage Activation/drug effectsMicroglia/drug effects*Minocycline/pharmacology*NADPH Oxidase/antagonists & inhibitors*Neurons/drug effects*Neuroprotective Agents*Nitric Oxide Synthase Type II/biosynthesisRatsRats, Sprague-DawleyReactive Oxygen Species/metabolismReverse Transcriptase Polymerase Chain ReactionSubstantia Nigra/drug effects*Thrombin/antagonists & inhibitors*
DOI
10.1111/j.1471-4159.2005.03503.x
PMID
16219027
Appears in Collections:
Journal Papers > Research Organization > Institute for Medical Sciences
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
김, 승업진, 병관
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