当前位置: X-MOL 学术Folia Neuropathol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Icariin ameliorates the cognitive function in an epilepsy neonatal rat model by blocking the GluR2/ERK I/II pathway
Folia Neuropathologica ( IF 1.5 ) Pub Date : 2020-10-21 , DOI: 10.5114/fn.2020.100067
Ying Guo 1 , Yuxiang Cai 2 , Xiaoge Zhang 1
Affiliation  

The present study was performed to evaluate the protective effects of icariin on cognitive function in a hypoxia-induced neonatal epilepsy rat model. Neonatal epilepsy was induced in rat pups on postnatal day (PD) 20 by induction of hypoxia for 15 minutes. Rats were treated intraperitoneally with icariin at 75 mg/kg 1 hour before the induction of hypoxia. The effects of icariin were examined by estimating seizure stage, cognitive function and parameters of electroencephalography (EEG) in this neonatal epilepsy rat model. Parameters of oxidative stress and expression of proteins were examined in the brain tissue of the neonatal epilepsy rat model by histopathological study and Western blotting analysis, respectively. The results of this study suggest that treatment with icariin ameliorates the changes in seizure stage, number of seizures and parameters of EEG in hypoxia-induced neonatal epilepsy rats. Oxidative stress and apoptosis were decreased in the brain tissue of the icariin treatment group compared to the hypoxia group. Moreover, treatment with icariin ameliorated the altered expression of glutamate ionotropic receptor AMPA type subunit 2 (GluR2) and extracellular receptor kinase (ERK I/II) proteins in the brain tissue of hypoxia-induced epilepsy rats. Histopathological study also showed that icariin treatment improved the histopathology of brain tissue of hypoxia-induced epilepsy rats. In conclusion, the results of the present study suggest that icariin protects against neuronal injury and improves cognitive function in hypoxia-induced neonatal epilepsy rats by modulating the GluR2/ERK I/II pathway.

中文翻译:

淫羊藿苷通过阻断 GluR2/ERK I/II 通路改善癫痫新生大鼠模型的认知功能

本研究旨在评估淫羊藿苷对缺氧诱导的新生儿癫痫大鼠模型认知功能的保护作用。在出生后第 20 天 (PD) 20 通过诱导缺氧 15 分钟在大鼠幼崽中诱导新生儿癫痫。在诱导缺氧前1小时,用75mg/kg淫羊藿苷腹膜内处理大鼠。通过估计该新生儿癫痫大鼠模型的癫痫发作阶段、认知功能和脑电图 (EEG) 参数来检查淫羊藿苷的作用。分别通过组织病理学研究和蛋白质印迹分析在新生癫痫大鼠模型的脑组织中检测氧化应激参数和蛋白质表达。这项研究的结果表明,淫羊藿苷治疗可以改善癫痫发作阶段的变化,缺氧诱导的新生癫痫大鼠癫痫发作次数和脑电图参数。与缺氧组相比,淫羊藿苷治疗组脑组织的氧化应激和细胞凋亡减少。此外,淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织中谷氨酸离子型受体AMPA 2型(GluR2)和细胞外受体激酶(ERK I/II)蛋白的表达改变。组织病理学研究还表明,淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织的组织病理学。总之,本研究的结果表明淫羊藿苷通过调节 GluR2/ERK I/II 通路来防止神经元损伤并改善缺氧诱导的新生癫痫大鼠的认知功能。与缺氧组相比,淫羊藿苷治疗组脑组织的氧化应激和细胞凋亡减少。此外,淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织中谷氨酸离子型受体AMPA 2型(GluR2)和细胞外受体激酶(ERK I/II)蛋白的表达改变。组织病理学研究还表明,淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织的组织病理学。总之,本研究的结果表明淫羊藿苷通过调节 GluR2/ERK I/II 通路来防止神经元损伤并改善缺氧诱导的新生癫痫大鼠的认知功能。与缺氧组相比,淫羊藿苷治疗组脑组织的氧化应激和细胞凋亡减少。此外,淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织中谷氨酸离子型受体AMPA 2型(GluR2)和细胞外受体激酶(ERK I/II)蛋白的表达改变。组织病理学研究还表明,淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织的组织病理学。总之,本研究的结果表明淫羊藿苷通过调节 GluR2/ERK I/II 通路来防止神经元损伤并改善缺氧诱导的新生癫痫大鼠的认知功能。淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织中谷氨酸离子型受体 AMPA 型亚基 2 (GluR2) 和细胞外受体激酶 (ERK I/II) 蛋白的表达改变。组织病理学研究还表明,淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织的组织病理学。总之,本研究的结果表明淫羊藿苷通过调节 GluR2/ERK I/II 通路来防止神经元损伤并改善缺氧诱导的新生癫痫大鼠的认知功能。淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织中谷氨酸离子型受体 AMPA 型亚基 2 (GluR2) 和细胞外受体激酶 (ERK I/II) 蛋白的表达改变。组织病理学研究还表明,淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织的组织病理学。总之,本研究的结果表明淫羊藿苷通过调节 GluR2/ERK I/II 通路来防止神经元损伤并改善缺氧诱导的新生癫痫大鼠的认知功能。组织病理学研究还表明,淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织的组织病理学。总之,本研究的结果表明淫羊藿苷通过调节 GluR2/ERK I/II 通路来防止神经元损伤并改善缺氧诱导的新生癫痫大鼠的认知功能。组织病理学研究还表明,淫羊藿苷治疗改善了缺氧诱导的癫痫大鼠脑组织的组织病理学。总之,本研究的结果表明淫羊藿苷通过调节 GluR2/ERK I/II 通路来防止神经元损伤并改善缺氧诱导的新生癫痫大鼠的认知功能。
更新日期:2020-10-30
down
wechat
bug