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托吡酯在大鼠脊髓损伤模型中作为神经保护剂的作用

Topiramate as a neuroprotective agent in a rat model of spinal cord injury.

作者信息

Narin Firat, Hanalioglu Sahin, Ustun Huseyin, Kilinc Kamer, Bilginer Burcak

机构信息

Department of Neurosurgery, Hacettepe University Faculty of Medicine, Ankara, Turkey.

Department of Pathology, Ankara Training and Research Hospital, Ankara, Turkey.

出版信息

Neural Regen Res. 2017 Dec;12(12):2071-2076. doi: 10.4103/1673-5374.221164.

DOI:10.4103/1673-5374.221164
PMID:29323048
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5784357/
Abstract

Topiramate (TPM) is a widely used antiepileptic and antimigraine agent which has been shown to exert neuroprotective effects in various experimental traumatic brain injury and stroke models. However, its utility in spinal cord injury has not been studied extensively. Thus, we evaluated effects of TPM on secondary cellular injury mechanisms in an experimental rat model of traumatic spinal cord injury (SCI). After rat models of thoracic contusive SCI were established by free weight-drop method, TPM (40 mg/kg) was given at 12-hour intervals for four times orally. Post TPM treatment, malondialdehyde and protein carbonyl levels were significantly reduced and reduced glutathione levels were increased, while immunoreactivity for endothelial nitric oxide synthase, inducible nitric oxide synthase, and apoptotic peptidase activating factor 1 was diminished in SCI rats. In addition, TPM treatment improved the functional recovery of SCI rats. This study suggests that administration of TPM exerts neuroprotective effects on SCI.

摘要

托吡酯(TPM)是一种广泛使用的抗癫痫和抗偏头痛药物,已被证明在各种实验性创伤性脑损伤和中风模型中发挥神经保护作用。然而,其在脊髓损伤中的效用尚未得到广泛研究。因此,我们评估了TPM对创伤性脊髓损伤(SCI)实验大鼠模型继发性细胞损伤机制的影响。通过自由落体法建立大鼠胸段挫伤性SCI模型后,每隔12小时口服TPM(40mg/kg),共4次。TPM治疗后,SCI大鼠的丙二醛和蛋白质羰基水平显著降低,还原型谷胱甘肽水平升高,而内皮型一氧化氮合酶、诱导型一氧化氮合酶和凋亡肽酶激活因子1的免疫反应性降低。此外,TPM治疗改善了SCI大鼠的功能恢复。本研究表明,给予TPM对SCI具有神经保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae2f/5784357/2df587df36cd/NRR-12-2071-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae2f/5784357/2ad3d8bf133b/NRR-12-2071-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae2f/5784357/5419ec7e6b23/NRR-12-2071-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae2f/5784357/f910adb7b091/NRR-12-2071-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae2f/5784357/2df587df36cd/NRR-12-2071-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae2f/5784357/2ad3d8bf133b/NRR-12-2071-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae2f/5784357/5419ec7e6b23/NRR-12-2071-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae2f/5784357/f910adb7b091/NRR-12-2071-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae2f/5784357/2df587df36cd/NRR-12-2071-g005.jpg

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Effects of antiepileptic drugs on antioxidant and oxidant molecular pathways: focus on trace elements.抗癫痫药物对抗氧化和氧化分子途径的影响:重点关注微量元素。
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