Free radicals are involved in continuous activation of nonreceptor tyrosine protein kinase c-Src after ischemia/reperfusion in rat hippocampus

Jun Guo, Fanjie Meng, Guangyi Zhang, Quanguang Zhang

Research output: Contribution to journalArticle

16 Scopus citations


NMDA receptor-mediated calcium over-loading and the following free radical generation play essential roles in cerebral ischemia lesion, leading to neuronal cell apoptosis or necrosis through complicated intracellular signaling cascades. Here we evaluated the effects of NMDA receptor antagonist (ketamine) and antioxidant (N-acetylcysteine) on ischemia- and reperfusion-induced activation of tyrosine kinase c-Src. The in vitro kinase assay showed that the ischemia-induced rapid activation of c-Src reached its peak at 5 min, and the reperfusion-induced continuous activation of c-Src reached another peak at 6 h reperfusion after 15 min ischemia (4.2 and 3.0 fold vs. sham control, respectively). Ketamine might suppress both peaks described above, but N-acetylcysteine, a free radical scavenger, was only able to partly reduce the peak activation elicited by 6 h reperfusion. These results suggest that free radical production is involved in NMDA receptor-mediated continuous activation of c-Src during ischemia/reperfusion but not that during ischemia.

Original languageEnglish (US)
Pages (from-to)101-104
Number of pages4
JournalNeuroscience Letters
Issue number2
Publication statusPublished - Jul 17 2003
Externally publishedYes



  • Activation
  • Autophosphorylation
  • Cerebral ischemia
  • Ketamine
  • N-Acetylcysteine
  • c-Src

ASJC Scopus subject areas

  • Neuroscience(all)

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