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异丙酚调节缺血性脑卒中中小胶质细胞激活的作用机制

Mechanisms of Action of Propofol in Modulating Microglial Activation in Ischemic Stroke.

作者信息

Abdolmohammadi Pouria, Bietar Bashir, Zhou Juan, Lehmann Christian

机构信息

Department of Microbiology and Immunology, Dalhousie University, Halifax, NS B2H 0A3, Canada.

Department of Pharmacology, Dalhousie University, Halifax, NS B2H 0A3, Canada.

出版信息

Molecules. 2025 Jun 28;30(13):2795. doi: 10.3390/molecules30132795.

DOI:10.3390/molecules30132795
PMID:40649310
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12251451/
Abstract

Ischemic stroke, responsible for the majority of stroke cases worldwide, triggers profound neuroinflammatory responses largely mediated by microglia. Excessive activation of pro-inflammatory microglia exacerbates neuronal injury, highlighting the need for therapeutic strategies targeting microglial modulation. Propofol (2,6-diisopropylphenol), a widely used intravenous anesthetic, has emerged as a promising neuroprotective agent due to its potent anti-inflammatory properties. This review comprehensively explores the diverse cellular mechanisms by which propofol attenuates microglial activation and inflammation in ischemic stroke. By elucidating these molecular pathways, it underscores the therapeutic potential of propofol in mitigating ischemic brain injury and guiding future clinical interventions.

摘要

缺血性中风是全球大多数中风病例的病因,它引发了主要由小胶质细胞介导的深刻神经炎症反应。促炎性小胶质细胞的过度激活会加剧神经元损伤,这凸显了针对小胶质细胞调节的治疗策略的必要性。丙泊酚(2,6-二异丙基苯酚)是一种广泛使用的静脉麻醉剂,由于其强大的抗炎特性,已成为一种有前景的神经保护剂。这篇综述全面探讨了丙泊酚减轻缺血性中风中小胶质细胞激活和炎症的多种细胞机制。通过阐明这些分子途径,它强调了丙泊酚在减轻缺血性脑损伤方面的治疗潜力,并为未来的临床干预提供指导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/193e/12251451/6ca439df9915/molecules-30-02795-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/193e/12251451/6ca439df9915/molecules-30-02795-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/193e/12251451/6ca439df9915/molecules-30-02795-g001.jpg

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Molecules. 2025 Jun 28;30(13):2795. doi: 10.3390/molecules30132795.
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本文引用的文献

1
Global, regional, and national burden of ischemic stroke, 1990-2021: an analysis of data from the global burden of disease study 2021.1990 - 2021年全球、区域和国家缺血性卒中负担:基于2021年全球疾病负担研究数据的分析
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Effect of General Anesthetic Agents on Microglia.
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Connexin 43 Phosphorylation: Implications in Multiple Diseases.连接蛋白 43 磷酸化:多种疾病的影响。
Molecules. 2023 Jun 22;28(13):4914. doi: 10.3390/molecules28134914.
5
Propofol inhibits neuroinflammation and metabolic reprogramming in microglia and .丙泊酚抑制小胶质细胞中的神经炎症和代谢重编程。
Front Pharmacol. 2023 Jun 13;14:1161810. doi: 10.3389/fphar.2023.1161810. eCollection 2023.
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Calcium/Calmodulin-Stimulated Protein Kinase II (CaMKII): Different Functional Outcomes from Activation, Depending on the Cellular Microenvironment.钙/钙调蛋白依赖性蛋白激酶 II(CaMKII):根据细胞微环境的不同,激活产生不同的功能结果。
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Propofol ameliorates ischemic brain injury by blocking TLR4 pathway in mice.丙泊酚通过阻断小鼠TLR4信号通路减轻缺血性脑损伤。
Transl Neurosci. 2022 Sep 1;13(1):246-254. doi: 10.1515/tnsci-2022-0238. eCollection 2022 Jan 1.
8
Inflammatory Responses After Ischemic Stroke.缺血性中风后的炎症反应。
Semin Immunopathol. 2022 Sep;44(5):625-648. doi: 10.1007/s00281-022-00943-7. Epub 2022 Jun 29.
9
JAK2/STAT3 Axis Intermediates Microglia/Macrophage Polarization During Cerebral Ischemia/Reperfusion Injury.JAK2/STAT3 轴介导体细胞/巨噬细胞极化在脑缺血/再灌注损伤中的作用。
Neuroscience. 2022 Aug 1;496:119-128. doi: 10.1016/j.neuroscience.2022.05.016. Epub 2022 May 20.
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miR-221/222 as biomarkers and targets for therapeutic intervention on cancer and other diseases: A systematic review.miR-221/222作为癌症及其他疾病治疗干预的生物标志物和靶点:一项系统综述
Mol Ther Nucleic Acids. 2022 Feb 11;27:1191-1224. doi: 10.1016/j.omtn.2022.02.005. eCollection 2022 Mar 8.