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Neuroprotective Effects of Lacosamide and Memantine on Hyperoxic Brain Injury in Rats.
Neurochemical Research ( IF 4.4 ) Pub Date : 2020-05-22 , DOI: 10.1007/s11064-020-03056-5
İpek Polat 1 , Serap Cilaker Mıcılı 2 , Meryem Çalışır 3 , Erhan Bayram 1 , Uluç Yiş 1 , Müge Ayanoğlu 1 , Derya Okur 1 , Pınar Edem 1 , Cem Paketçi 1 , Kazım Tuğyan 2 , Osman Yılmaz 3 , Semra Hız Kurul 1
Affiliation  

In neonates supraphysiological oxygen therapy has been demonstrated to cause neuronal death in hippocampus, prefrontal cortex, parietal cortex, and retrosplenial cortex. There is a need for the detection of novel neuroprotective drugs. Neuroprotective effects of lacosamide or memantine have been demonstrated in adult patients with ischemia, trauma and status epilepticus. The effects in immature brains may be different. This study aimed to evaluate neuroprotective effects of lacosamide and memantine treatment in a hyperoxia-induced brain injury model in immature rats. This study was performed in the Animal Experiments Laboratory of Dokuz Eylul University Faculty of Medicine. Neonatal Wistar strain rat pups were exposed to hyperoxia (80% oxygen + 20% nitrogen) for five days postnatally. They were divided into five groups; hyperoxia + lacosamide, hyperoxia + memantine, hyperoxia + lacosamide and memantine, hyperoxia + saline, control groups. After termination of the experiment, brain tissues were examined. Neuron counting in examined regions were found to be higher in hyperoxia + memantine and hyperoxia + lacosamide and memantine groups than hyperoxia + saline group. The presence of apoptotic cells evaluated with TUNEL and active Caspase-3 in hyperoxia + memantine and hyperoxia + lacosamide and memantine groups were found to be lower compared to hyperoxia + saline group. This study demonstrates that neuron death and apoptosis in newborn rat brains after hyperoxia is reduced upon memantine treatment. This is the first study to show the effects of memantine and lacosamide on hyperoxia-induced damage in neonatal rat brains.

中文翻译:

Lacosamide和美金刚胺对大鼠高氧性脑损伤的神经保护作用。

在新生儿中,超生理氧疗法已被证明可导致海马,前额叶皮层,顶叶皮层和脾后皮层神经元死亡。需要检测新型神经保护药物。在患有局部缺血,外伤和癫痫持续状态的成年患者中,已证明了拉考酰胺或美金刚的神经保护作用。对未成熟大脑的影响可能有所不同。这项研究旨在评估在未成熟大鼠高氧血症引起的脑损伤模型中拉考酰胺和美金刚治疗的神经保护作用。这项研究是在Dokuz Eylul大学医学院的动物实验实验室中进行的。新生Wistar品系大鼠幼鼠在出生后五天暴露于高氧环境(80%氧气+ 20%氮气)。他们分为五个组。高氧+拉考酰胺 高氧+美金刚,高氧+拉考酰胺和美金刚,高氧+生理盐水,对照组。实验终止后,检查脑组织。发现高氧+美金刚和高氧+拉可酰胺和美金刚组的神经元计数高于高氧+盐水组。发现高氧+美金刚和高氧+拉考酰胺和美金刚组中用TUNEL和活性Caspase-3评估的凋亡细胞的含量低于高氧+盐水组。这项研究表明,在美金刚治疗后,高氧后新生大鼠大脑中神经元的死亡和凋亡减少。这是第一项显示美金刚和拉考酰胺对高氧血症引起的新生大鼠脑损伤的影响的研究。高氧+生理盐水,对照组。实验终止后,检查脑组织。发现高氧+美金刚和高氧+拉可酰胺和美金刚组的神经元计数高于高氧+生理盐水组。发现高氧+美金刚和高氧+拉考酰胺和美金刚组中用TUNEL和活性Caspase-3评估的凋亡细胞的含量低于高氧+盐水组。这项研究表明,在美金刚治疗后,高氧后新生大鼠大脑中神经元的死亡和凋亡减少。这是第一项显示美金刚和拉考酰胺对高氧血症引起的新生大鼠脑损伤的影响的研究。高氧+生理盐水,对照组。实验终止后,检查脑组织。发现高氧+美金刚和高氧+拉可酰胺和美金刚组的神经元计数高于高氧+生理盐水组。发现高氧+美金刚和高氧+拉考酰胺和美金刚组中用TUNEL和活性Caspase-3评估的凋亡细胞的含量低于高氧+盐水组。这项研究表明,在美金刚治疗后,高氧后新生大鼠大脑中神经元的死亡和凋亡减少。这是第一项显示美金刚和拉考酰胺对高氧血症引起的新生大鼠脑损伤的影响的研究。发现高氧+美金刚和高氧+拉可酰胺和美金刚组的神经元计数高于高氧+生理盐水组。发现高氧+美金刚和高氧+拉考酰胺和美金刚组中用TUNEL和活性Caspase-3评估的凋亡细胞的含量低于高氧+盐水组。这项研究表明,在美金刚治疗后,高氧后新生大鼠大脑中神经元的死亡和凋亡减少。这是第一项显示美金刚和拉考酰胺对高氧血症引起的新生大鼠脑损伤的影响的研究。发现高氧+美金刚和高氧+拉可酰胺和美金刚组的神经元计数高于高氧+生理盐水组。发现高氧+美金刚和高氧+拉考酰胺和美金刚组中用TUNEL和活性Caspase-3评估的凋亡细胞的含量低于高氧+盐水组。这项研究表明,在美金刚治疗后,高氧后新生大鼠大脑中神经元的死亡和凋亡减少。这是第一项显示美金刚和拉考酰胺对高氧血症引起的新生大鼠脑损伤的影响的研究。发现高氧+美金刚和高氧+拉考酰胺和美金刚组中用TUNEL和活性Caspase-3评估的凋亡细胞的含量低于高氧+盐水组。这项研究表明,在美金刚治疗后,高氧后新生大鼠大脑中神经元的死亡和凋亡减少。这是第一项显示美金刚和拉考酰胺对高氧血症引起的新生大鼠脑损伤的影响的研究。发现高氧+美金刚和高氧+拉考酰胺和美金刚组中用TUNEL和活性Caspase-3评估的凋亡细胞的含量低于高氧+盐水组。这项研究表明,在美金刚治疗后,高氧后新生大鼠大脑中神经元的死亡和凋亡减少。这是第一项显示美金刚和拉考酰胺对高氧血症引起的新生大鼠脑损伤的影响的研究。
更新日期:2020-05-22
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