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不同轻度缺氧处理对大鼠海马区红藻氨酸诱导性癫痫发作的影响。

Effect of different mild hypoxia manipulations on kainic acid-induced seizures in the hippocampus of rats.

机构信息

Department of Neurosurgery, Xijing Hospital, The Fourth Military Medical University, 17 West Changle Road, Xi'an 710032, China.

出版信息

Neurochem Res. 2013 Jan;38(1):123-32. doi: 10.1007/s11064-012-0899-6. Epub 2012 Oct 12.

DOI:10.1007/s11064-012-0899-6
PMID:23065181
Abstract

The protective effect of the mild hypoxia to the epilepsy has been widely tested. Although it is found that the hypoxia protects the brain by up-regulation of hypoxia-inducible factor-1α, few focused on systematic comparisons between different mild hypoxia manipulations and their effects. The male Sprague-Dawley rats were observed following exposure to hypoxia before and after epilepsy for 3 days with 90 min per day. The effects of different mild hypoxia manipulations on kainic acid-induced epilepsy were compared from the perspective of morphology, molecular biology and behavioral test. Results showed that different mild hypoxia manipulations could inhibit the cell apoptosis of kainic acid-induced rat hippocampus and improve their physiological functions. The effect of preconditioning group was better than that of postconditioning group and that of preconditioning and postconditioning with mild hypoxia group was the best among all the groups. The result showed that the preconditioning and postconditioning of mild hypoxia was recommended pre- and post-epilepsy and exposure to mild hypoxia should be prolonged. These findings might provide new ideas and methods for the clinical treatment of epilepsy.

摘要

轻度缺氧对癫痫的保护作用已得到广泛验证。虽然已经发现缺氧通过上调缺氧诱导因子-1α来保护大脑,但很少有研究关注不同轻度缺氧处理及其作用之间的系统比较。雄性 Sprague-Dawley 大鼠在癫痫发作前和发作后每天暴露于 90 分钟的缺氧中观察 3 天。从形态学、分子生物学和行为测试的角度比较了不同轻度缺氧处理对红藻氨酸诱导癫痫的影响。结果表明,不同的轻度缺氧处理可以抑制红藻氨酸诱导的大鼠海马细胞凋亡,改善其生理功能。预处理组的效果优于后处理组,而轻度缺氧预处理和后处理组的效果是所有组中最好的。结果表明,推荐在癫痫发作前和发作后进行轻度缺氧预处理和后处理,并延长暴露于轻度缺氧的时间。这些发现可能为癫痫的临床治疗提供新的思路和方法。

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Neurochem Res. 2013 Jan;38(1):123-32. doi: 10.1007/s11064-012-0899-6. Epub 2012 Oct 12.
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