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Direct protection of cultured neurons from ischemia-like injury by minocycline.

Authors
  • Huang, Wendy C1
  • Qiao, Yanli
  • Xu, Lijun
  • Kacimi, Rachid
  • Sun, Xiaoyun
  • Giffard, Rona G
  • Yenari, Midori A
  • 1 Department of Neurology, University of California, San Francisco and the San Francisco Veterans Affairs Medical Center, San Francisco, CA 94121, USA.
Type
Published Article
Journal
Anatomy & cell biology
Publication Date
Dec 01, 2010
Volume
43
Issue
4
Pages
325–331
Identifiers
DOI: 10.5115/acb.2010.43.4.325
PMID: 21267407
Source
Medline
Keywords
License
Unknown

Abstract

Minocycline, a tetracycline antibiotic, is now known to protect cells via an anti-inflammatory mechanism. We further explored this effect using an in vitro model of ischemia-like injury to neurons. Coculturing neurons with microglia, the brain's resident immune cell, modestly increased cell death due to oxygen and glucose deprivation (OGD), compared to neurons alone. Treatment of cocultures with minocycline decreased cell death to a level significantly lower than that of neurons alone. Treatment of cocultures with minocycline or inhibitors of various immune mediators, also led to decreased cell death. Importantly, treatment of neuron cultures without added microglia with these same inhibitors of tissue plasminogen activator, matrix metalloproteinases, TNF-alpha and inducible nitric oxide synthase as well as minocycline also led to decreased cell death. Thus, anti-inflammatory treatments appear to be directly protective of neurons from in vitro ischemia.

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