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白杨素通过抑制氧化应激和过渡元素来保护海马体免受脑缺血再灌注损伤。

Chrysin protects against cerebral ischemia-reperfusion injury in hippocampus via restraining oxidative stress and transition elements.

机构信息

School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, China.

Department of Pharmacy, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, China.

出版信息

Biomed Pharmacother. 2023 May;161:114534. doi: 10.1016/j.biopha.2023.114534. Epub 2023 Mar 16.

Abstract

Chrysin is a natural flavonoid compound that has antioxidant and neuroprotective effects. Cerebral ischemia reperfusion (CIR) is closely connected with increased oxidative stress in the hippocampal CA1 region and homeostasis disorder of transition elements such as iron (Fe), copper (Cu) and zinc (Zn). This exploration was conducted to elucidate the antioxidant and neuroprotective effects of chrysin based on transient middle cerebral artery occlusion (tMCAO) in rats. Experimentally, sham group, model group, chrysin (50.0 mg/kg) group, Ginaton (21.6 mg/kg) group, Dimethyloxallyl Glycine (DMOG, 20.0 mg/kg) + chrysin group and DMOG group were devised. The rats in each group were performed to behavioral evaluation, histological staining, biochemical kit detection, and molecular biological detection. The results indicated that chrysin restrained oxidative stress and the rise of transition element levels, and regulated transition element transporter levels in tMCAO rats. DMOG activated hypoxia-inducible factor-1 subunit alpha (HIF-1α), reversed the antioxidant and neuroprotective effects of chrysin, and increased transition element levels. In a word, our findings emphasize that chrysin plays a critical role in protecting CIR injury via inhibiting HIF-1α against enhancive oxidative stress and raised transition metal levels.

摘要

白杨素是一种天然黄酮类化合物,具有抗氧化和神经保护作用。脑缺血再灌注(CIR)与海马 CA1 区氧化应激增加以及铁(Fe)、铜(Cu)和锌(Zn)等过渡元素的内稳态紊乱密切相关。本研究旨在基于大鼠短暂性大脑中动脉闭塞(tMCAO)探讨白杨素的抗氧化和神经保护作用。实验中设计了假手术组、模型组、白杨素(50.0mg/kg)组、金纳多(21.6mg/kg)组、二甲基乙二醛(DMOG,20.0mg/kg)+白杨素组和 DMOG 组。每组大鼠进行行为评价、组织学染色、生化试剂盒检测和分子生物学检测。结果表明,白杨素抑制 tMCAO 大鼠的氧化应激和过渡元素水平升高,并调节过渡元素转运体水平。DMOG 激活缺氧诱导因子-1 亚基α(HIF-1α),逆转了白杨素的抗氧化和神经保护作用,并增加了过渡元素水平。总之,我们的研究结果强调,白杨素通过抑制 HIF-1α 对抗增强的氧化应激和升高的过渡金属水平,在保护 CIR 损伤中发挥重要作用。

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