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用于监测大脑炎症氧化还原状态的影像生物标志物

Imaging Biomarkers for Monitoring the Inflammatory Redox Landscape in the Brain.

作者信息

Fernandes Eduardo Felipe Alves, Özcelik Dennis

机构信息

Department of Drug Design and Pharmacology, University of Copenhagen, Universitetsparken 2, 2100 Copenhagen, Denmark.

Chemistry | Biology | Pharmacy Information Center, ETH Zürich, Vladimir-Prelog-Weg 10, 8093 Zürich, Switzerland.

出版信息

Antioxidants (Basel). 2021 Mar 28;10(4):528. doi: 10.3390/antiox10040528.

DOI:10.3390/antiox10040528
PMID:33800685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8065574/
Abstract

Inflammation is one key process in driving cellular redox homeostasis toward oxidative stress, which perpetuates inflammation. In the brain, this interplay results in a vicious cycle of cell death, the loss of neurons, and leakage of the blood-brain barrier. Hence, the neuroinflammatory response fuels the development of acute and chronic inflammatory diseases. Interrogation of the interplay between inflammation, oxidative stress, and cell death in neurological tissue in vivo is very challenging. The complexity of the underlying biological process and the fragility of the brain limit our understanding of the cause and the adequate diagnostics of neuroinflammatory diseases. In recent years, advancements in the development of molecular imaging agents addressed this limitation and enabled imaging of biomarkers of neuroinflammation in the brain. Notable redox biomarkers for imaging with positron emission tomography (PET) tracers are the 18 kDa translocator protein (TSPO) and monoamine oxygenase B (MAO-B). These findings and achievements offer the opportunity for novel diagnostic applications and therapeutic strategies. This review summarizes experimental as well as established pharmaceutical and biotechnological tools for imaging the inflammatory redox landscape in the brain, and provides a glimpse into future applications.

摘要

炎症是促使细胞氧化还原稳态走向氧化应激的关键过程之一,而氧化应激会使炎症持续存在。在大脑中,这种相互作用会导致细胞死亡、神经元丧失和血脑屏障渗漏的恶性循环。因此,神经炎症反应会推动急性和慢性炎症性疾病的发展。在体内对神经组织中炎症、氧化应激和细胞死亡之间的相互作用进行研究极具挑战性。潜在生物学过程的复杂性以及大脑的脆弱性限制了我们对神经炎症性疾病病因的理解和充分诊断。近年来,分子成像剂开发方面的进展克服了这一限制,并能够对大脑中的神经炎症生物标志物进行成像。用于正电子发射断层扫描(PET)示踪剂成像的重要氧化还原生物标志物是18 kDa转运蛋白(TSPO)和单胺氧化酶B(MAO-B)。这些发现和成果为新型诊断应用和治疗策略提供了机会。本综述总结了用于成像大脑炎症氧化还原态势的实验性以及已有的药物和生物技术工具,并对未来应用进行了展望。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8065574/499e202959dc/antioxidants-10-00528-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8065574/20a19cb177c2/antioxidants-10-00528-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8065574/144e01a94c29/antioxidants-10-00528-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8065574/499e202959dc/antioxidants-10-00528-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8065574/20a19cb177c2/antioxidants-10-00528-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8065574/144e01a94c29/antioxidants-10-00528-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8065574/499e202959dc/antioxidants-10-00528-g003.jpg

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