Balanophora polyandra多糖通过PI3K/AKT/mTOR信号通路增强神经元自噬,从而改善自然衰老小鼠的脑功能衰退。

IF 1.6 4区 医学 Q4 NEUROSCIENCES Neuroreport Pub Date : 2024-04-10 DOI:10.1097/wnr.0000000000002024
Wenyan Zhong, Jingjing Chen, Yumin He, Li Xiao, Chengfu Yuan
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引用次数: 0

摘要

大脑神经元衰退是各种神经退行性疾病的主要原因。本研究旨在探讨巴兰多糖(BPP)对衰老相关神经元退化的影响。用常规饲料喂养 C57BL/6 小鼠 27 个月,以建立自然衰老小鼠模型。从 3 个月大开始,药物治疗组的小鼠分别用含 0.05% 或 0.18% BPP 的饲料喂养至 27 个月大。评估了 BPP 治疗对小鼠大脑神经元病理变化的影响,以及自噬相关蛋白和信号通路蛋白的影响。BPP治疗对自然衰老小鼠大脑皮层和海马神经元的病理损伤有显著的积极影响,缓解了神经元变性,增强了Nissl体的染色。此外,BPP还能上调衰老小鼠皮层和海马中的自噬相关蛋白LC3 II/I、Parkin和PINK1,并显著降低p62、PI3K、p-蛋白激酶B(AKT)和p-mTOR的表达。免疫荧光结果显示,自然衰老小鼠脑中主要与NeuN共表达的LC3亮度降低,而BPP治疗后观察到LC3阳性神经元增加。总之,BPP治疗可通过PI3K/AKT/mTOR信号转导增强神经元自噬,从而改善自然衰老小鼠的脑功能退化。这些发现表明,BPP 有可能减轻或延缓与衰老相关的神经退行性病变,但还需要进一步研究以验证其在老年人群中的疗效。
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The polysaccharides from Balanophora polyandra enhanced neuronal autophagy to ameliorate brain function decline in natural aging mice through the PI3K/AKT/mTOR signaling pathway.
The decline of aging brain neurons is the main cause of various neurodegenerative disease. This study aimed to examine the impact of Balanophora polyandra polysaccharides (BPP) against aging related neuronal deterioration. C57BL/6 mice were fed with regular feed for 27 months to establish a natural aging mouse model. From 3 months of age, mice in the drug-treated group were respectively fed with feed containing 0.05 or 0.18% BPP until 27 months of age. The effects of BPP treatment on the pathological changes of neurons in mice brain were evaluated, as well as autophagy-related and signaling pathway proteins. BPP treatment had a notable positive impact on the pathological injury of cortical and hippocampal neurons, alleviated neuronal degeneration, and enhanced the staining of Nissl bodies in natural aging mice. Furthermore, BPP upregulated autophagy-related proteins LC3 II/I, Parkin, and PINK1 in the cortex and hippocampus of aging mice, and significantly decreased the expression of p62, PI3K, p-protein Kinase B (AKT), and p-mTOR. Immunofluorescence results showed a reduction in the brightness of LC3, which mainly coexpressed with NeuN in natural aging mice brain, and increased LC3-positive neurons were observed after BPP treatment. Collectively, BPP treatment enhanced neuronal autophagy to improve brain functional degradation through the PI3K/AKT/mTOR signaling in natural aging mice. These finding suggested that BPP has potential to mitigate or delay the neurodegeneration associated with aging and further investigation was needed to validate its efficacy in elderly populations.
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来源期刊
Neuroreport
Neuroreport 医学-神经科学
CiteScore
3.20
自引率
0.00%
发文量
150
审稿时长
1 months
期刊介绍: NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.
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