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[Cell injury and its protection in astrocytes].

Abstract
Incubation of cultured astrocytes in Ca(2+)-containing medium after exposure to Ca(2+)-free medium causes Ca2+ influx followed by delayed cell death. Here, we summarize the mechanisms underlying the Ca(2+)-mediated injury of cultured astrocytes and the protective effects of drugs against Ca(2+)-reperfusion injury. Our results show that Ca(2+)-reperfusion injury of astrocytes appears to be mediated by apoptosis as evidenced by DNA fragmentation and nuclear condensation. Calpain, reactive oxygen species (ROS) production, calcineurin, caspase-3, and NF-kappa B activation are involved in Ca(2+)-reperfusion injury. Several drugs including T-588 and idebenone protect astrocytes against Ca(2+)-reperfusion injury. The protective effect of idebenone is mediated by nerve growth factor production, whereas that of T-588 is mediated mainly by the mitogen-activated protein/extracellular signal-regulated kinase signal cascade.
AuthorsT Matsuda, K Takuma, E Lee, A Baba
JournalNihon yakurigaku zasshi. Folia pharmacologica Japonica (Nihon Yakurigaku Zasshi) Vol. 114 Issue 5 Pg. 281-6 (Nov 1999) ISSN: 0015-5691 [Print] Japan
PMID10621941 (Publication Type: English Abstract, Journal Article, Review)
Chemical References
  • Benzoquinones
  • Ubiquinone
  • Calpain
  • idebenone
  • Calcium
Topics
  • Animals
  • Apoptosis (physiology)
  • Astrocytes (drug effects, physiology)
  • Benzoquinones (pharmacology)
  • Calcium (pharmacology)
  • Calpain (pharmacology)
  • Cell Death
  • Cells, Cultured
  • Humans
  • Reperfusion Injury (pathology)
  • Ubiquinone (analogs & derivatives)

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