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Kainic Acid‐Induced Oxidative Injury Is Attenuated by Hypoxic Preconditioning
Author(s) -
WANG CHENGHAO,
CHANG ANYU,
TSAI MAYJYWAN,
CHENG HENRICH,
LIAO LIPING,
LIN ANYA MAANYUH
Publication year - 2005
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1338.054
Subject(s) - kainic acid , glutathione , oxidative stress , chemistry , lipid peroxidation , neuroprotection , pharmacology , superoxide dismutase , glutathione peroxidase , reactive oxygen species , endocrinology , hypoxia (environmental) , tunel assay , medicine , apoptosis , biochemistry , biology , glutamate receptor , oxygen , enzyme , receptor , organic chemistry
A bstract : 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.