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首页> 外文期刊>CNS neuroscience & therapeutics. >Protective effects of leonurine against ischemic stroke in mice by activating nuclear factor erythroid 2‐related factor 2 pathway
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Protective effects of leonurine against ischemic stroke in mice by activating nuclear factor erythroid 2‐related factor 2 pathway

机译：激活神经核因子红系2相关因子2通路对小鼠体内缺血性中风的保护作用

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Aims Leonurine has been shown to trigger antioxidant responses during ischemic stroke, and nuclear factor erythroid 2‐related factor 2 (Nrf‐2) imparts protective effects against oxidative injury. The present study has determined that leonurine prevents ischemic injury of brain tissues via Nrf‐2 pathway activation. Methods Male ICR mice and Nrf‐2sup?/?/sup mice were subjected to permanent middle cerebral artery occlusion (pMCAO) and received leonurine treatment at 2?hours after pMCAO by intraperitoneal injection. Neurological deficit scores as well as infarct volume were assessed to determine the neuroprotective role of leonurine. Nrf‐2 was investigated using Western blotting and real‐time polymerase chain reaction (RT‐PCR) analysis to elucidate the neuroprotective mechanism of leonurine. Commercial kits were employed to determine reactive oxygen species (ROS), superoxide (SOD), catalase (CAT), glutathione peroxidase (GSH‐Px), malonaldehyde (MDA), and glutathione (GSH). Vascular endothelial growth factor (VEGF) was evaluated by Western blotting and RT‐PCR analysis, and VEGF was localized using immunofluorescence. Results The application of leonurine on ICR mice resulted in an improvement in neurological deficit scores and a reduction in infarct volume. Leonurine upregulated nuclear Nrf‐2 protein and increased total Nrf‐2 protein expression and mRNA levels. Leonurine regulated SOD, MDA, CAT, GSH, and GSH‐Px, and it significantly inhibited ROS production in ICR mice. Leonurine improved VEGF expression and increased VEGF expression in neurons, astrocytes, and endothelial cells. However, leonurine had no obvious beneficial effects on Nrf‐2sup?/?/sup mice. Conclusions Leonurine exerted neuroprotective effects, promoted antioxidant responses, and upregulated VEGF expression by activating the Nrf‐2 pathway.
机译：目的是证明Leonurine在缺血性中风时会触发抗氧化反应，而核因子红系2相关因子2（Nrf-2）则具有抗氧化损伤的保护作用。本研究已经确定，Leonurine可通过Nrf-2途径激活来预防脑组织的缺血性损伤。方法对雄性ICR小鼠和Nrf-2 ？/？小鼠进行永久性大脑中动脉闭塞（pMCAO），并于pMCAO后2小时通过腹腔注射对小鼠进行尿酸治疗。评估神经功能缺损评分和梗塞体积，以确定leonurine的神经保护作用。使用蛋白质印迹和实时聚合酶链反应（RT-PCR）分析对Nrf-2进行了研究，以阐明亮氨酸的神经保护机制。使用商业试剂盒测定活性氧（ROS），超氧化物（SOD），过氧化氢酶（CAT），谷胱甘肽过氧化物酶（GSH-Px），丙二醛（MDA）和谷胱甘肽（GSH）。通过Western印迹和RT-PCR分析评估血管内皮生长因子（VEGF），并使用免疫荧光法定位VEGF。结果在ICR小鼠上使用leururine可以改善神经功能缺损评分并减少梗塞体积。益母草碱上调了核Nrf-2蛋白并增加了总Nrf-2蛋白表达和mRNA水平。益母草碱调节SOD，MDA，CAT，GSH和GSH-Px，并显着抑制ICR小鼠的ROS产生。益母草嘌呤改善神经元，星形胶质细胞和内皮细胞中VEGF的表达并增加VEGF的表达。然而，Leonurine对Nrf-2 ？/？小鼠没有明显的有益作用。结论Leonurine通过激活Nrf-2途径发挥神经保护作用，促进抗氧化反应并上调VEGF表达。

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