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咖啡因及其在缺血性事件中的神经保护作用:一种依赖于腺苷受体的机制。

Caffeine and Its Neuroprotective Role in Ischemic Events: A Mechanism Dependent on Adenosine Receptors.

机构信息

Neurobiology of the Retina Laboratory, Biomedical Sciences Program, Biomedical Institute, Fluminense Federal University, Niterói, RJ, Brazil.

Neurobiology of the Retina Laboratory, Program of Neurosciences, Institute of Biology, Fluminense Federal University, Niterói, RJ, Brazil.

出版信息

Cell Mol Neurobiol. 2022 Aug;42(6):1693-1725. doi: 10.1007/s10571-021-01077-4. Epub 2021 Mar 17.

DOI:10.1007/s10571-021-01077-4
PMID:33730305
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11421760/
Abstract

Ischemia is characterized by a transient, insufficient, or permanent interruption of blood flow to a tissue, which leads to an inadequate glucose and oxygen supply. The nervous tissue is highly active, and it closely depends on glucose and oxygen to satisfy its metabolic demand. Therefore, ischemic conditions promote cell death and lead to a secondary wave of cell damage that progressively spreads to the neighborhood areas, called penumbra. Brain ischemia is one of the main causes of deaths and summed with retinal ischemia comprises one of the principal reasons of disability. Although several studies have been performed to investigate the mechanisms of damage to find protective/preventive interventions, an effective treatment does not exist yet. Adenosine is a well-described neuromodulator in the central nervous system (CNS), and acts through four subtypes of G-protein-coupled receptors. Adenosine receptors, especially A and A receptors, are the main targets of caffeine in daily consumption doses. Accordingly, caffeine has been greatly studied in the context of CNS pathologies. In fact, adenosine system, as well as caffeine, is involved in neuroprotection effects in different pathological situations. Therefore, the present review focuses on the role of adenosine/caffeine in CNS, brain and retina, ischemic events.

摘要

缺血是指组织的血液供应短暂、不足或永久性中断,导致葡萄糖和氧气供应不足。神经组织高度活跃,它密切依赖葡萄糖和氧气来满足其代谢需求。因此,缺血条件会促进细胞死亡,并导致细胞损伤的二次波逐渐扩散到周围区域,称为半影区。脑缺血是死亡的主要原因之一,与视网膜缺血一起构成了残疾的主要原因之一。尽管已经进行了多项研究来探讨损伤机制以寻找保护/预防干预措施,但目前还没有有效的治疗方法。腺苷是中枢神经系统 (CNS) 中一种描述良好的神经调节剂,通过四种 G 蛋白偶联受体亚型发挥作用。腺苷受体,特别是 A1 和 A2A 受体,是咖啡因在日常消费剂量中的主要靶点。因此,咖啡因在 CNS 病理情况下已得到广泛研究。事实上,腺苷系统以及咖啡因参与了不同病理情况下的神经保护作用。因此,本综述重点介绍了腺苷/咖啡因在中枢神经系统、大脑和视网膜缺血事件中的作用。

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