Protective effect of minocycline on oxygen/glucose deprivation and NMDA-induced neurotoxicity in rat primary neurons and hippocampal slices.
- Author:
Wei HE
1
;
Er-qing WEI
;
Meng-ling WANG
;
Lu-ying LIU
;
Zhong CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Hypoxia; Cells, Cultured; Dizocilpine Maleate; pharmacology; Glucose; metabolism; Hippocampus; drug effects; Male; Minocycline; pharmacology; N-Methylaspartate; toxicity; Neurons; drug effects; Neuroprotective Agents; pharmacology; Rats; Rats, Sprague-Dawley
- From: Journal of Zhejiang University. Medical sciences 2004;33(3):219-224
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo develop oxygen/glucose deprivation (OGD)-and NMDA-induced neurotoxicity models in rat primary neurons and hippocampal slices, and to determine the protective effect of minocycline.
METHODSThe injuries of primary neurons were induced by OGD or NMDA (50micromol/L). Morphological changes of neurons were observed, and neuron viability was evaluated by MTT assay. The changes of light transmittance (LT) were induced by OGD or NMDA in rat hippocampal slices. The effects of minocycline and MK-801, an NMDA receptor antagonist, were observed in the models of OGD-or NMDA-induced injuries.
RESULTMinocycline concentration dependently inhibited OGD induced decrease of neuron viability and ameliorated neuron morphological changes at 1 and 10 micromol/L. It also inhibited NMDA insult at 10 and 100 micromol/L. MK-801 inhibited both injuries at 1 micromol/L. However, minocycline at 1 or 10 micromol/L did not inhibit the augment of LT in hippocampal slices induced by OGD or NMDA, while MK-801 inhibited both OGD-and NMDA-induced LT augments.
CONCLUSIONMinocycline protects neurons from OGD insult, which may inhibit NMDA receptor-mediated neurotoxicity through an indirect pathway, but has no effect on OGD-or NMDA-induced immediate injury in hippocampal slices.
