神经保护:抗炎药的途径

Patrice Mendel Nzogang, M. Donkeng
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引用次数: 1

摘要

神经元是神经系统的基本结构和功能单位,其主要功能是整合和解释神经元输入或信息。神经细胞的寿命通常贯穿于个体的一生。然而,一些生理或病理过程可能影响神经元,导致该细胞或组织过早死亡。这种由病理环境引起的神经系统过早死亡就是我们所说的神经毒性。用以解释神经毒性的生化机制尚不完全清楚。然而,无论其机制如何,其结果通常是细胞凋亡、热致死或坏死。这些机制的例子包括兴奋性毒性、氧化应激、胶质细胞破坏、血管中断和炎症。利用药理学手段保护神经元免受损伤的想法导致了神经保护概念的诞生。这一新概念是基于正在进行的研究而出现的,表明可以通过物理和药理学手段通过上述机制预防或避免神经毒性,但血管中断机制除外。在本章中,我们将简要介绍与神经毒性有关的炎症机制,并提出可能对神经保护的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neuroprotection: The Way of Anti-Inflammatory Agents
Neurons are basic structural and functional units of the nervous system with major function being that of integration and interpretation of neuronal input or information. The lifespan of a nerve cell generally last throughout the individual lifetime. However, some physiologic or pathologic processes may affect the neuron causing premature death of this cell or tissue. This premature neurological death caused by pathologic circumstances is what we call neurotoxicity. The biochemical mechanisms put forward to explain neurotoxicity are not fully known. Nonetheless, whatever the mechanism involved, the outcome usually results in apoptosis, pyropoptosis, or necrosis. Examples of these mechanisms include excitotoxicity, oxidative stress, glial cell destruction, vascular interruptions, and inflammation. The idea about possibly protecting neurons against insults using pharmacologic means leads to the birth of the neuroprotection concept. This new concept has emerged based on ongoing research, suggesting it is possible through physical and pharmacological means to prevent or avoid neurotoxicity by the abovementioned mechanisms but with the exception of vascular interruption mechanisms. We will present in this chapter a synoptic view of the inflammatory mechanisms implicated in neurotoxicity and bring out the possible implications in neuroprotection.
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