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脂肪酸乙醇酰胺在哮喘中的分子靶点。

Molecular Targets of Fatty Acid Ethanolamides in Asthma.

机构信息

Vladivostok Branch of Federal State Budgetary Science Institution «Far Eastern Scientific Center of Physiology and Pathology of Respiration-Institute of Medical Climatology and Rehabilitative Treatment, Russkaya st. 73g, 690105 Vladivostok, Russia.

出版信息

Medicina (Kaunas). 2019 Apr 1;55(4):87. doi: 10.3390/medicina55040087.

DOI:10.3390/medicina55040087
PMID:30939862
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6524029/
Abstract

Asthma is a common allergic pathology of the respiratory tract that requires the study of mechanisms underlying it, due to severe forms of the disease, which are refractory to therapy. The review is devoted to the search for molecular targets of fatty acid ethanolamides in asthma, in particular palmitoylethanolamide (PEA), which has been successfully used in the treatment of chronic inflammatory and neurodegenerative diseases, in the pathogenesis of which the nervous and immune systems are involved. Recently, the potentially important role of neuro-immune interactions in the development of allergic reactions has been established. Many of the clinical symptoms accompanying allergic airway inflammation are the result of the activation of neurons in the airways, so the attention of researchers is currently focused on neuro-immune interactions, which can play an important role in asthma pathophysiology. A growing number of scientific works confirm that the key molecule in the implementation of these inter-systemic interactions is nerve growth factor (NGF). In addition to its classic role in nervous system physiology, NGF is considered as an important factor associated with the pathogenesis of allergic diseases, particularly asthma, by regulating of mast cell differentiation. In this regard, NGF can be one of the targets of PEA in asthma therapy. PEA has a biological effect on the nervous system, and affects the activation and the degranulation of mast cells.

摘要

哮喘是一种常见的呼吸道过敏性疾病,由于疾病的严重形式对治疗有抗性,因此需要研究其发病机制。本综述致力于寻找脂肪酸乙醇酰胺在哮喘中的分子靶点,特别是棕榈酸乙醇酰胺(PEA),它已成功用于治疗慢性炎症和神经退行性疾病,其中神经系统和免疫系统参与了发病机制。最近,神经免疫相互作用在过敏反应发展中的潜在重要作用已经得到证实。许多伴随过敏性气道炎症的临床症状是气道神经元激活的结果,因此研究人员目前的注意力集中在神经免疫相互作用上,它可能在哮喘病理生理学中发挥重要作用。越来越多的科学研究证实,实施这些系统间相互作用的关键分子是神经生长因子(NGF)。除了其在神经系统生理学中的经典作用外,NGF 还被认为是与过敏疾病,特别是哮喘发病机制相关的重要因素,通过调节肥大细胞分化。在这方面,NGF 可以成为 PEA 在哮喘治疗中的靶点之一。PEA 对神经系统具有生物学作用,并影响肥大细胞的激活和脱颗粒。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b416/6524029/d8156c897641/medicina-55-00087-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b416/6524029/ab332a6eda41/medicina-55-00087-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b416/6524029/749b386743f8/medicina-55-00087-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b416/6524029/d8156c897641/medicina-55-00087-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b416/6524029/ab332a6eda41/medicina-55-00087-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b416/6524029/749b386743f8/medicina-55-00087-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b416/6524029/d8156c897641/medicina-55-00087-g003.jpg

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Ultra-micronized palmitoylethanolamide rescues the cognitive decline-associated loss of neural plasticity in the neuropathic mouse entorhinal cortex-dentate gyrus pathway.超微化棕榈酸乙醇酰胺可挽救神经病理性小鼠内嗅皮层-齿状回通路认知功能下降相关的神经可塑性丧失。
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Peroxisome Proliferator-Activated Receptors as a Therapeutic Target in Asthma.过氧化物酶体增殖物激活受体作为哮喘的治疗靶点
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Anti-Inflammatory Effects of Fucoxanthinol in LPS-Induced RAW264.7 Cells through the NAAA-PEA Pathway.脂氧合酶抑制剂通过 NAAA-PEA 通路抑制脂多糖诱导的 RAW264.7 细胞炎症反应
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