白藜芦醇对缺血性脑损伤的神经保护作用

IF 1.6 Q3 CLINICAL NEUROLOGY
NeuroSci Pub Date : 2021-09-01 DOI:10.3390/neurosci2030022
Noelia D Machado, Gorka Villena Armas, M. A. Fernández, S. Grijalvo, D. Díaz Díaz
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引用次数: 3

摘要

脑缺血是导致成人死亡的第三大原因和致残的第一大原因。这一过程是由于大脑大动脉闭塞导致脑血流量水平下降所致。这种血液供应的限制会导致低水平的氧气和葡萄糖,从而导致细胞能量代谢的减少,产生炎症,最终导致神经系统恶化。目前,血流恢复是治疗缺血性脑卒中唯一有效的方法。然而,仍有相当一部分患者预后较差,这可能与损伤组织再灌注过程中活性氧(ROS)的生成增加有关。氧化应激和炎症可以通过调节线粒体功能来避免,并且已被确定为脑缺血治疗的潜在靶点。近年来,类黄酮和多酚类化合物对脑血管疾病的有益作用被广泛研究。大量研究表明,使用白藜芦醇(RSV)可显著减少脑缺血引起的脑损伤。根据体外和体内实验,越来越多的证据表明RSV参与cAMP/AMPK/SIRT1调控、JAK/ERK/STAT信号通路调控、TLR4信号转导调控、肠/脑轴调控、GLUT3上调抑制、神经元自噬激活、新生SUR1表达抑制等多种途径。在这篇综述中,我们总结了基于RSV本身和RSV负载纳米颗粒在体外和体内模型中的神经保护作用的最新结果,重点关注这种作用机制,并描述了RSV在缺血性脑损伤病例中发挥积极作用的潜在治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neuroprotective Effects of Resveratrol in Ischemic Brain Injury
Cerebral ischemia represents the third cause of death and the first cause of disability in adults. This process results from decreasing cerebral blood flow levels as a result of the occlusion of a major cerebral artery. This restriction in blood supply generates low levels of oxygen and glucose, which leads to a decrease in the energy metabolism of the cell, producing inflammation, and finally, neurological deterioration. Currently, blood restoration of flow is the only effective approach as a therapy in terms of ischemic stroke. However, a significant number of patients still have a poor prognosis, probably owing to the increase in the generation of reactive oxygen species (ROS) during the reperfusion of damaged tissue. Oxidative stress and inflammation can be avoided by modulating mitochondrial function and have been identified as potential targets for the treatment of cerebral ischemia. In recent years, the beneficial actions of flavonoids and polyphenols against cerebrovascular diseases have been extensively investigated. The use of resveratrol (RSV) has been shown to markedly decrease brain damage caused by ischemia in numerous studies. According to in vitro and in vivo experiments, there is growing evidence that RSV is involved in several pathways, including cAMP/AMPK/SIRT1 regulation, JAK/ERK/STAT signaling pathway modulation, TLR4 signal transduction regulation, gut/brain axis modulation, GLUT3 up-regulation inhibition, neuronal autophagy activation, and de novo SUR1 expression inhibition. In this review, we summarize the recent outcomes based on the neuroprotective effect of RSV itself and RSV-loaded nanoparticles in vitro and in vivo models focusing on such mechanisms of action as well as describing the potential therapeutic strategies in which RSV plays an active role in cases of ischemic brain injury.
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