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地锦草乙醇提取物对慢性脑灌注不足的神经保护作用：通过调节System Xc-/谷胱甘肽/谷胱甘肽过氧化物酶4轴减轻氧化应激和铁死亡

Neuroprotective effects of ethanol extraction from Diels on chronic cerebral hypoperfusion: modulation of the System Xc-/GSH/GPX4 axis to alleviate oxidative stress and ferroptosis.

作者信息

Cheng Jianghao, Ma Xiaoxia, Tao Jie, Jiang Xiaoli, Chen Pu, Duan Xiaohua

机构信息

Yunnan Key Laboratory of Dai and Yi Medicines, Yunnan University of Chinese Medicine, Kunming, Yunnan, China.

出版信息

Front Pharmacol. 2025 Feb 25;16:1552228. doi: 10.3389/fphar.2025.1552228. eCollection 2025.

DOI:10.3389/fphar.2025.1552228
PMID:40070574
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11893507/
Abstract

INTRODUCTION

Vascular dementia (VD) is a neurodegenerative disease caused by chronic cerebral hypoperfusion (CCH), which considerably impact patients' quality of life. Ethanol extraction from (RY-A) has gained attention for its potential neuroprotective effects, but its effects and mechanisms of action on CCH are unknown.

METHODS

After 30 days of RY-A gavage treatment in a CCH rat model, its effects were evaluated using the Morris water maze test, cerebral blood flow measurements, and HE staining of the brain. These findings, combined with serum medicinal chemistry, RNA-seq, and metabolomics analyses, revealed the active compounds and mechanisms of RY-A in CCH rats. The results were further validated using assay kits and Western blot techniques.

RESULTS

RY-A treatment significantly attenuated neurological damage and improved cognitive function in CCH rats. Ultra-high-performance liquid chromatography high-resolution mass spectrometry identified 511 blood-entry compounds of RY-A. RNA-seq and metabolomic analysis showed that RY-A might help to normalize changes in gene and metabolite expression caused by CCH. RY-A induced neuroprotective effects by increasing the production of key proteins involved in ferroptosis inhibition, such as SLC7A11, SLC3A2, GSS, and GPX4, while increasing antioxidant enzyme activities and alleviating oxidative stress.

CONCLUSION

RY-A inhibited oxidative stress and ferroptosis by activating the System Xc-/GSH/GPX4 pathway and balancing iron metabolism, thereby attenuating CCH-induced neurological damage and cognitive deficits.

摘要

引言

血管性痴呆（VD）是一种由慢性脑灌注不足（CCH）引起的神经退行性疾病，对患者的生活质量有相当大的影响。从[植物名称]中提取的乙醇提取物（RY-A）因其潜在的神经保护作用而受到关注，但其对CCH的作用及其作用机制尚不清楚。

方法

在CCH大鼠模型中进行30天的RY-A灌胃治疗后，使用莫里斯水迷宫试验、脑血流测量和脑HE染色评估其效果。这些发现，结合血清药物化学、RNA测序和代谢组学分析，揭示了RY-A在CCH大鼠中的活性成分和作用机制。使用检测试剂盒和蛋白质免疫印迹技术进一步验证了结果。

结果

RY-A治疗显著减轻了CCH大鼠的神经损伤并改善了认知功能。超高效液相色谱-高分辨率质谱法鉴定出RY-A的511种入血成分。RNA测序和代谢组学分析表明，RY-A可能有助于使由CCH引起的基因和代谢物表达变化正常化。RY-A通过增加参与铁死亡抑制的关键蛋白如SLC7A11、SLC3A2、GSS和GPX4的产生，同时增加抗氧化酶活性并减轻氧化应激，从而诱导神经保护作用。

结论

RY-A通过激活系统Xc-/谷胱甘肽/谷胱甘肽过氧化物酶4途径并平衡铁代谢来抑制氧化应激和铁死亡，从而减轻CCH诱导的神经损伤和认知缺陷。

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