Kainic acid-induced oxidative injury is attenuated by hypoxic preconditioning

Cheng Hao Wang, Anyu Chang, May Jywan Tsai, Henrich Cheng, Li Ping Liao, Anya Maan Yuh Lin*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Female Wistar rats were subjected to 380 mmHg in an altitude chamber for 15 h/day for 28 days. Hypoxic preconditioning attenuated kainic acid (KA)-induced oxidative injury, including KA-elevated lipid peroxidation and neuronal loss in rat hippocampus. Furthermore, KA-induced translocation of cytochrome c and apoptosis-inducing factor from mitochondria to cytosol was attenuated in the hypoxic rats. In addition, hypoxic preconditioning attenuated the KA-induced reduction in glutathione content and superoxide dismutase as well as KA-induced increase in glutathione peroxidase. Although local infusion of KA increased hippocampal NF-κB binding activity in the normoxic rat, hypoxia further enhanced KA-elevated NF-κB binding activity. Moreover, hypoxic preconditioning potentiated the KA-induced increase in Bcl-2 level in the lesioned hippocampus. Our data suggest that hypoxic preconditioning exerts its neuroprotection of KA-induced oxidative injury via enhancing NF-κB activation, upregulating the antioxidative defense system, and attenuating the apoptotic process.

Original languageEnglish
Pages (from-to)314-324
Number of pages11
JournalAnnals of the New York Academy of Sciences
StatePublished - 2005


  • Apoptosis
  • Bcl-2
  • Hypoxic preconditioning
  • Kainate
  • NF-κB


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