摘要
背景:乙醇是已知有两γγ-氨基丁酸受体激动剂和拮抗剂特性类似-N-甲基-D-天门冬氨酸常用挥发性麻醉药。最近的证据表明自噬能减少乙醇所致神经毒性的发生。最近的研究发现,全麻可导致线粒体形态发生的长期损害和在发育中的大鼠脑内突触传递,两者都伴随着增强的自噬活动。自噬在全麻介导的神经毒性中起重要作用。 方法:本文概述了自噬在麻醉相关神经毒性发展中的作用,包括自噬在神经细胞存活和死亡中的作用,以及自噬在神经细胞存活和死亡中的作用。麻醉剂与神经元自噬的关系及全麻药诱导神经自噬激活的分子和细胞机制G脑和潜在的治疗方法,旨在调节自噬途径。 结果:在一种时间和浓度依赖性的模式下,全麻药可以破坏细胞内钙稳态,从而增强自噬和凋亡激活。n度自噬与凋亡之间的相互作用可能最终决定了耳蜗细胞的损伤。与某些麻醉剂有关的钙流量的增加很可能会扰乱lys。染色体功能。这导致体内溶酶体贩运过度激活,导致线粒体损伤,活性氧物种增加,脂质过氧化。 结论:自噬可能在麻醉相关神经毒性的发生中起一定作用。了解这一点可能会导致旨在预防或改善全麻的策略或疗法。抽动素介导的神经毒性。
关键词: 未成熟的大脑,全身麻醉剂,自噬,神经毒性,乙醇,神经细胞。
Current Medicinal Chemistry
Title:Anesthetic Agents and Neuronal Autophagy. What We Know and What We Don't.
Volume: 25 Issue: 8
关键词: 未成熟的大脑,全身麻醉剂,自噬,神经毒性,乙醇,神经细胞。
摘要: Background: Ethanol is known to have both γ-Aminobutyric acid agonist and Nmethyl- D-aspartate antagonist characteristics similar to commonly used volatile anesthetic agents. Recent evidence demonstrates that autophagy can reduce the development of ethanol induced neurotoxicity. Recent studies have found that general anesthesia can cause longterm impairment of both mitochondrial morphogenesis and synaptic transmission in the developing rat brain, both of which are accompanied by enhanced autophagy activity. Autophagy may play an important role in general anesthetic mediated neurotoxicity.
Methods: This review outlines the role of autophagy in the development of anesthetic related neurotoxicity and includes an explanation of the role of autophagy in neuronal cell survival and death, the relationship between anesthetic agents and neuronal autophagy, possible molecular and cellular mechanisms underlying general anesthetic agent induced activation of neuronal autophagy in the developing brain, and potential therapeutic approaches aimed at modulating autophagic pathways.
Results: In a time- and concentration-dependent pattern, general anesthetic agents can disrupt intracellular calcium homeostasis which enhances both autophagy and apoptosis activation. The degree of neural cell injury may be ultimately determined by the interplay between autophagy and apoptosis. It appears likely that the increase in calcium flux associated with some anesthetic agents disrupts lysosomal function. This results in an over-activation of endosomal- lysosomal trafficking causing mitochondrial damage, reactive oxygen species upregulation, and lipid peroxidation.
Conclusion: Autophagy may play a role in the development of anesthetic related neurotoxicity. Understanding this may lead to strategies or therapies aimed at preventing or ameliorating general anesthetic agent mediated neurotoxicity.
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Cite this article as:
Anesthetic Agents and Neuronal Autophagy. What We Know and What We Don't., Current Medicinal Chemistry 2018; 25 (8) . https://dx.doi.org/10.2174/0929867324666171009123605
DOI https://dx.doi.org/10.2174/0929867324666171009123605 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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