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金丝桃苷通过增强抗氧化水平和减少自噬来减轻癫痫引起的神经元损伤。

Hyperoside alleviates epilepsy-induced neuronal damage by enhancing antioxidant levels and reducing autophagy.

机构信息

Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou University, Yangzhou, 225001, PR China; Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, 225001, PR China; Jiangsu Key Laboratory of Experimental & Translational Non-coding RNA Research, Yangzhou, 225001, PR China.

Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou University, Yangzhou, 225001, PR China; Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, 225001, PR China; Jiangsu Key Laboratory of Experimental & Translational Non-coding RNA Research, Yangzhou, 225001, PR China; Department of Neurology, Affiliated Hospital, Yangzhou University, 225001, PR China; Jiangsu Key Laboratory of Zoonosis, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine of Yangzhou University, Yangzhou, 225009, PR China.

出版信息

J Ethnopharmacol. 2020 Jul 15;257:112884. doi: 10.1016/j.jep.2020.112884. Epub 2020 Apr 18.

DOI:10.1016/j.jep.2020.112884
PMID:32311482
Abstract

ETHNOPHARMACOLOGICAL RELEVANCE

Hypericum perforatum L. (genus Hypericum, family Hypericaceae), a plant commonly used in traditional Chinese medicine, is believed to confer a wide range of benefits, including fever reduction, detoxification, calming, and pain relief via decoctions of its stems and leaves. Hyperoside (HYP), a natural compound extracted from Hypericum perforatum L., has been shown to demonstrate a wide array of bioactivities including antioxidative, anti-inflammatory, and anti-apoptotic effects. In this study, we investigated the effects of HYP on epilepsy-induced neuronal damage in mice and the associated regulatory factors.

AIM OF THE STUDY

This study examined the potential therapeutic use of HYP for the treatment of neuronal damage in a mouse model of epilepsy and explored the relationships of the potential neuroprotective effects of HYP pretreatment with antioxidant levels and autophagy.

MATERIALS AND METHODS

ICR mice were randomly divided into six groups: sham group, sham-HYP group, KA group, KA-HYP group, KA-HYP-DDC group and KA-CQ group. Immunohistochemical staining was used to assess changes in NeuN, IBA-1, and GFAP expression in the CA3 region of the hippocampus. Immunofluorescence staining was used to assess the effects of HYP on the number of autophagosomes that accumulated in neurons in the hippocampal CA3 region. The levels of SOD1, SOD2, LC3I/II, Beclin1, and PI3K/AKT and MAPK signaling-related proteins were detected by Western blot.

RESULTS

Pretreatment with 50 mg/kg HYP protected against epilepsy-induced neuronal damage in the hippocampal CA3 region. Additionally, HYP enhanced antioxidant levels and reduced the levels of autophagy-related proteins via the PI3K/AKT and MAPK pathways.

CONCLUSION

HYP protected the hippocampal CA3 region against epilepsy-induced neuronal damage via enhancing antioxidant levels and reducing autophagy. The mechanism of action may be related to the maintenance of antioxidant levels and the suppression of autophagy via the PI3K/Akt and MAPK pathways.

摘要

民族药理学相关性

贯叶金丝桃 L.(贯叶金丝桃属,金丝桃科),一种常用于中药的植物,被认为具有广泛的益处,包括通过煎煮其茎和叶来降低体温、解毒、镇静和缓解疼痛。金丝桃苷(HYP)是从贯叶金丝桃 L. 中提取的一种天然化合物,已显示出广泛的生物活性,包括抗氧化、抗炎和抗细胞凋亡作用。在这项研究中,我们研究了 HYP 对小鼠癫痫诱导神经元损伤的影响及其相关调节因子。

研究目的

本研究旨在探讨 HYP 治疗癫痫小鼠模型神经元损伤的潜在治疗用途,并探讨 HYP 预处理的潜在神经保护作用与抗氧化水平和自噬的关系。

材料和方法

ICR 小鼠随机分为六组:假手术组、假手术-HYP 组、KA 组、KA-HYP 组、KA-HYP-DDC 组和 KA-CQ 组。免疫组织化学染色用于评估海马 CA3 区 NeuN、IBA-1 和 GFAP 表达的变化。免疫荧光染色用于评估 HYP 对海马 CA3 区神经元中自噬体积累数量的影响。Western blot 检测 SOD1、SOD2、LC3I/II、Beclin1、PI3K/AKT 和 MAPK 信号相关蛋白的水平。

结果

50mg/kg HYP 预处理可预防癫痫诱导的海马 CA3 区神经元损伤。此外,HYP 通过 PI3K/AKT 和 MAPK 通路增强抗氧化水平并降低自噬相关蛋白的水平。

结论

HYP 通过增强抗氧化水平和减少自噬来保护海马 CA3 区免受癫痫诱导的神经元损伤。其作用机制可能与通过 PI3K/Akt 和 MAPK 通路维持抗氧化水平和抑制自噬有关。

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