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Kainic Acid-Induced Oxidative Injury Is Attenuated by Hypoxic Preconditioning

机译:Kainic酸诱导的氧化损伤通过缺氧预处理衰减

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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.
机译:女性Wistar大鼠在高度室中进行380mmHg,持续15小时/天28天。缺氧预处理减毒酸(Ka)诱导氧化损伤,包括Ka升高的脂质过氧化和大鼠海马的神经元损失。此外,在缺氧大鼠中,KA诱导的细胞色素C和细胞凋亡诱导因子与线粒体到细胞溶溶胶的易位。此外,缺氧预处理减弱了谷胱甘肽含量和超氧化物歧化酶的显着降低以及谷胱甘肽过氧化物酶的Ka诱导的增加。虽然KA局部输注增加了常氧大鼠的海马NF-κB结合活性,但缺氧进一步增强了KA升高的NF-κB结合活性。此外,缺氧预处理激增了损伤海马的Bcl-2水平的Ka诱导的升高。我们的数据表明,缺氧预处理通过增强NF-κB活化,上调抗氧化防御系统并衰减凋亡过程,缺氧预处理施加了KA诱导的氧化损伤。

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