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神经炎症机制与植物疗法干预:系统评价。

Neuroinflammation Mechanisms and Phytotherapeutic Intervention: A Systematic Review.

机构信息

Drug Discovery and Development Laboratory, Department of Chemistry, University of Delhi, New Delhi-110007, India.

Dr. B. R. Ambedkar Center for Biomedical Research, University of Delhi, New Delhi-110007, India.

出版信息

ACS Chem Neurosci. 2020 Nov 18;11(22):3707-3731. doi: 10.1021/acschemneuro.0c00427. Epub 2020 Nov 4.

Abstract

Neuroinflammation is indicated in the pathogenesis of several acute and chronic neurological disorders. Acute lesions in the brain parenchyma induce intense and highly complex neuroinflammatory reactions with similar mechanisms among various disease prototypes. Microglial cells in the CNS sense tissue damage and initiate inflammatory responses. The cellular and humoral constituents of the neuroinflammatory reaction to brain injury contribute significantly to secondary brain damage and neurodegeneration. Inflammatory cascades such as proinflammatory cytokines from invading leukocytes and direct cell-mediated cytotoxicity between lymphocytes and neurons are known to cause "collateral damage" in models of acute brain injury. In addition to degeneration and neuronal cell loss, there are secondary inflammatory mechanisms that modulate neuronal activity and affect neuroinflammation which can even be detected at the behavioral level. Hence, several of health conditions result from these pathogenetic conditions which are underlined by progressive neuronal function loss due to chronic inflammation and oxidative stress. In the first part of this Review, we discuss critical neuroinflammatory mediators and their pathways in detail. In the second part, we review the phytochemicals which are considered as potential therapeutic molecules for treating neurodegenerative diseases with an inflammatory component.

摘要

神经炎症在几种急性和慢性神经疾病的发病机制中都有表现。大脑实质的急性病变会引发强烈而高度复杂的神经炎症反应,而各种疾病原型之间存在类似的机制。中枢神经系统中的小胶质细胞感知组织损伤并引发炎症反应。神经炎症反应对脑损伤的细胞和体液成分对继发性脑损伤和神经退行性变有重要贡献。在急性脑损伤模型中,已知炎症级联反应(如浸润白细胞中的促炎细胞因子和淋巴细胞与神经元之间的直接细胞介导的细胞毒性)会导致“附带损伤”。除了变性和神经元细胞丢失外,还有继发性炎症机制调节神经元活动并影响神经炎症,甚至在行为水平上也可以检测到。因此,由于慢性炎症和氧化应激导致神经元功能逐渐丧失,许多健康状况都是由这些发病机制引起的。在这篇综述的第一部分,我们详细讨论了关键的神经炎症介质及其途径。在第二部分,我们综述了被认为是具有抗炎成分的治疗神经退行性疾病的潜在治疗分子的植物化学物质。

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