解密蜂毒肽 Melittin 的神经保护作用:对机制相互作用的见解

IF 4.6 2区 医学 Q1 NEUROSCIENCES
Molecular Neurobiology Pub Date : 2025-07-01 Epub Date: 2025-03-04 DOI:10.1007/s12035-025-04808-6
Pankaj Kadyan, Lovedeep Singh
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引用次数: 0

摘要

神经退行性疾病,如阿尔茨海默病、帕金森病和多发性硬化症,其特征是神经元结构和功能的逐渐丧失。这些情况往往导致认知能力下降,运动功能障碍,并最终严重损害日常活动。神经退行性疾病的一个关键特征是慢性炎症,这有助于神经元损伤并加剧疾病进展。传统的治疗方法主要侧重于缓解症状,而不是解决根本原因,强调需要新的治疗方法。蜂毒素是一种从蜂毒中提取的生物活性肽,因其多方面的神经保护特性而受到关注,特别是在神经炎症和神经退行性疾病的背景下。本文将深入探讨蜂毒素发挥神经保护作用的分子机制,重点关注其调节神经炎症、细胞凋亡和神经发生的能力。研究表明蜂毒素通过抑制calpain介导的凋亡诱导因子和Bax的激活,下调促凋亡通路,从而减少神经元细胞死亡。此外,蜂毒素通过抑制神经炎症过程发挥其神经保护作用,特别是通过下调NF-κB和MAPK等关键炎症通路。这种调节导致促炎细胞因子和前列腺素的产生减少,这与神经退行性疾病的发病机制有关。除了抗炎作用外,蜂毒素还可能通过调节BDNF/Trk-B/CREB信号通路促进神经发生,这在神经元存活和可塑性中起着至关重要的作用。这些特性表明蜂毒素不仅可以缓解症状,还可以解决神经退行性疾病的根本原因,为开发新的神经退行性疾病治疗方法提供了一条有希望的途径。需要进一步的研究来验证其在临床环境中的有效性和安全性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Deciphering the Neuroprotective Action of Bee Venom Peptide Melittin: Insights into Mechanistic Interplay.

Neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis, are characterized by progressive loss of neuronal structure and function. These conditions often lead to cognitive decline, motor dysfunction, and ultimately severe impairment of daily activities. A key feature of neurodegenerative diseases is chronic inflammation, which contributes to neuronal damage and exacerbates disease progression. Traditional treatments mainly focus on symptomatic relief rather than addressing the underlying causes, highlighting the need for novel therapeutic approaches. Melittin, a bioactive peptide derived from bee venom, has garnered attention for its multifaceted neuroprotective properties, particularly in the context of neuroinflammatory and neurodegenerative disorders. This review delves into the molecular mechanisms through which melittin exerts neuroprotective effects, with a focus on its ability to modulate neuroinflammation, apoptosis, and neurogenesis. Research indicates that melittin can downregulate pro-apoptotic pathways by inhibiting calpain-mediated activation of apoptosis-inducing factor and Bax, thereby reducing neuronal cell death. Additionally, melittin exerts its neuroprotective effects through the inhibition of neuroinflammatory processes, specifically by downregulating key inflammatory pathways such as NF-κB and MAPK. This modulation leads to decreased production of proinflammatory cytokines and prostaglandins, which are implicated in the pathogenesis of neurodegenerative disorders. Beyond its anti-inflammatory actions, melittin promotes neurogenesis, potentially through the modulation of the BDNF/Trk-B/CREB signaling pathway, which plays a crucial role in neuronal survival and plasticity. These properties suggest that melittin not only provides symptomatic relief but could also address the root causes of neuronal degeneration, presenting a promising avenue for the development of new treatments for neurodegenerative diseases. Further research is required to validate its efficacy and safety in clinical settings.

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来源期刊
Molecular Neurobiology
Molecular Neurobiology 医学-神经科学
CiteScore
9.00
自引率
2.00%
发文量
480
审稿时长
1 months
期刊介绍: Molecular Neurobiology is an exciting journal for neuroscientists needing to stay in close touch with progress at the forefront of molecular brain research today. It is an especially important periodical for graduate students and "postdocs," specifically designed to synthesize and critically assess research trends for all neuroscientists hoping to stay active at the cutting edge of this dramatically developing area. This journal has proven to be crucial in departmental libraries, serving as essential reading for every committed neuroscientist who is striving to keep abreast of all rapid developments in a forefront field. Most recent significant advances in experimental and clinical neuroscience have been occurring at the molecular level. Until now, there has been no journal devoted to looking closely at this fragmented literature in a critical, coherent fashion. Each submission is thoroughly analyzed by scientists and clinicians internationally renowned for their special competence in the areas treated.
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