首页> 美国卫生研究院文献>International Journal of Molecular Sciences >The Neuroprotective Effect of Hericium erinaceus Extracts in Mouse Hippocampus after Pilocarpine-Induced Status Epilepticus
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The Neuroprotective Effect of Hericium erinaceus Extracts in Mouse Hippocampus after Pilocarpine-Induced Status Epilepticus

机译:毛状猴提取物对毛果芸香碱诱发的癫痫持续状态小鼠海马的神经保护作用

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摘要

Hericium erinaceus (HE), a culinary-medicinal mushroom, has shown therapeutic potential in many brain diseases. However, the role of HE in status epilepticus (SE)-mediated neuronal death and its underlying mechanisms remain unclear. We investigated the neuroprotective effects of HE using a pilocarpine-induced SE model. Male C57BL/6 mice received crude extracts of HE (60 mg/kg, 120 mg/kg, or 300 mg/kg, p.o.) for 21 d from 14 d before SE to 6 d after SE. At 7 d after SE, cresyl violet and immunohistochemistry of neuronal nuclei revealed improved hippocampal neuronal survival in animals treated with 60 mg/kg and 120 mg/kg of HE, whereas those treated with 300 mg/kg of HE showed similar neuronal death to that of vehicle-treated controls. While seizure-induced reactive gliosis, assessed by immunohistochemistry, was not altered by HE, the number of hippocampal cyclooxygenase 2 (COX2)-expressing cells was significantly reduced by 60 and 120 mg/kg of HE. Triple immunohistochemistry demonstrated no overlap of COX2 labeling with Ox42, in addition to a decrease in COX2/GFAP-co-immunoreactivity in the group treated with 60 mg/kg HE, suggesting that the reduction of COX2 by HE promotes neuroprotection after SE. Our findings highlight the potential application of HE for preventing neuronal death after seizures.
机译:猴头菇(HE),一种烹饪药用蘑菇,已在许多脑部疾病中显示出治疗潜力。然而,HE在癫痫持续状态(SE)介导的神经元死亡及其潜在机制中的作用尚不清楚。我们使用毛果芸香碱诱导的SE模型研究了HE的神经保护作用。雄性C57BL / 6小鼠从SE前14天到SE后6天接受HE的粗提取物(60 mg / kg,120 mg / kg或300 mg / kg,p.o.)21天。 SE后第7天,甲酚紫和神经元核免疫组织化学分析显示,用60 mg / kg和120 mg / kg HE处理的动物海马神经元存活率提高,而用300 mg / kg HE处理的动物海马神经元存活率与之相似。车辆处理的控件。尽管通过免疫组织化学评估癫痫发作诱发的反应性神经胶质细胞增生并未改变,但表达海马环氧合酶2(COX2)的细胞数量却显着减少了60和120 mg / kg HE。三重免疫组化显示,用60 mg / kg HE治疗的组中COX2 / GFAP-co-免疫反应性降低,除了用Ox42标记COX2外没有重叠,这表明用HE降低COX2可以促进SE后的神经保护。我们的发现突出了HE在预防癫痫发作后神经元死亡中的潜在应用。

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