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青蒿素上调神经细胞黏附分子 L1 减轻小鼠脑出血后的神经功能缺损。

Artemisinin upregulates neural cell adhesion molecule L1 to attenuate neurological deficits after intracerebral hemorrhage in mice.

机构信息

Department of Neurosurgery, General Hospital of Xinjiang Military Region, Urumqi, China.

出版信息

Brain Behav. 2022 May;12(5):e2558. doi: 10.1002/brb3.2558. Epub 2022 Mar 29.

DOI:10.1002/brb3.2558
PMID:35349764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9120716/
Abstract

BACKGROUND AND PURPOSE

Intracerebral hemorrhage (ICH) is a subtype of stroke and results in neurological deficits in patients without any effective treatments. Artemisinin (ART), a well-known antimalarial Chinese medicine, exerts multiple essential roles in the central and peripheral nervous system due to its antioxidative and anti-inflammation properties. Neural cell adhesion molecule L1 (L1CAM, L1) is considered to be implicated in neural development, functional maintenance, and neuroprotection during disease. However, whether these two essential molecules are neuroprotective in ICH remains unclear.

METHODS

Therefore, the present study investigated the influence of ART on the recovery of neurological deficits in a mouse model of ICH induced by collagenase and the underlying mechanism.

RESULTS

It was revealed that ART is capable of upregulating L1 expression to alleviate brain edema, reduce oxidative stress, and inhibit inflammation to alleviate ICH-induced brain injury to improve the neurological outcome in mice suffering from ICH.

CONCLUSION

These results may lay the foundation for ART to be a novel candidate treatment for ICH.

摘要

背景与目的

脑出血(ICH)是中风的一种亚型,会导致患者出现神经功能缺损,目前尚无有效的治疗方法。青蒿素(ART)是一种著名的抗疟疾中药,由于其抗氧化和抗炎特性,在中枢和外周神经系统中发挥着多种重要作用。神经细胞黏附分子 L1(L1CAM,L1)被认为与神经发育、功能维持和疾病期间的神经保护有关。然而,这两种重要分子是否对 ICH 具有神经保护作用尚不清楚。

方法

因此,本研究探讨了 ART 对胶原酶诱导的 ICH 小鼠模型中神经功能缺损恢复的影响及其潜在机制。

结果

结果表明,ART 能够上调 L1 的表达,减轻脑水肿,减少氧化应激,抑制炎症,从而减轻 ICH 引起的脑损伤,改善 ICH 小鼠的神经功能预后。

结论

这些结果可能为 ART 成为治疗 ICH 的一种新的候选药物奠定基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d7/9120716/f198d9ae25c9/BRB3-12-e2558-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d7/9120716/e36874134d36/BRB3-12-e2558-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d7/9120716/9d2668673428/BRB3-12-e2558-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d7/9120716/01acca07a493/BRB3-12-e2558-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d7/9120716/f198d9ae25c9/BRB3-12-e2558-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d7/9120716/e36874134d36/BRB3-12-e2558-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d7/9120716/9d2668673428/BRB3-12-e2558-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d7/9120716/01acca07a493/BRB3-12-e2558-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d7/9120716/f198d9ae25c9/BRB3-12-e2558-g005.jpg

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