工程菌<italic style="font-style: italic">Clostridium butyricum</italic>-pMTL007-GLP-1通过PI3K/AKT/GSK-3β信号通路对A53T α-突触核蛋白小鼠模型的神经保护作用

方鑫; 王云; 龙贞莉; 廖宾; 王博; 洪道俊; 罗洁; 陈廷涛

doi:10.1631/jzus.B2500237

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工程菌Clostridium butyricum-pMTL007-GLP-1通过PI3K/AKT/GSK-3β信号通路对A53T α-突触核蛋白小鼠模型的神经保护作用

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Research Article | Updated：2026-08-13

工程菌Clostridium butyricum-pMTL007-GLP-1通过PI3K/AKT/GSK-3β信号通路对A53T α-突触核蛋白小鼠模型的神经保护作用
Neuroprotection of engineered Clostridium butyricum-pMTL007-GLP-1 in A53T α-synuclein (α-syn) mouse model via PI3K/AKT/GSK-3β
浙江大学学报（英文版）（B辑：生物医学和生物技术） 2026年27卷第8期页码：872-887
Affiliations：

1.Department of Neurology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China
2.Jiangxi Province Key Laboratory of Bioengineering Drugs, School of Pharmacy, Jiangxi Medical College, Nanchang University, Nanchang 330031, China
3.Institute of Neurology, Jiangxi Academy of Clinical Medical Science, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China
4.School of Queen Mary, Nanchang University, Nanchang 330031, China
5.Rare Disease Center, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China
6.Key Laboratory of Rare Neurological Diseases of Jiangxi Provincial Health Commission, Jiangxi Medical College, Nanchang University, Nanchang 330006, China
7.School of Public Health, Jiangxi Medical College, Nanchang University, Nanchang 330031, China
Funds：

the Jiangxi Provincial Natural Science Foundation(20242BAB26134;20242BAB25464);the Academic and Technical Leaders of Major Disciplines in Jiangxi Province(20213BCJL22049);the National Natural Science Foundation of China(82060222;82460237)
DOI：10.1631/jzus.B2500237
中图分类号：
CSTR：
收稿：2025-05-09，

修回：2025-07-21，

网络首发：2026-08-13，

纸质出版：2026-08-13
Accepted：

方鑫,王云,龙贞莉等.工程菌,Clostridium butyricum-pMTL007-GLP-1通过PI3K/AKT/GSK-3β信号通路对A53T α-突触核蛋白小鼠模型的神经保护作用[J].浙江大学学报（英文版）（B辑：生物医学和生物技术）,2026,27(08):872-887.

Xin FANG, Yun WANG, Zhenli LONG, et al. Neuroprotection of engineered Clostridium butyricum-pMTL007-GLP-1 in A53T α-synuclein (α-syn) mouse model via PI3K/AKT/GSK-3β[J]. Journal of Zhejiang University-SCIENCE B, 2026, 27(8): 872-887. DOI: 10.1631/jzus.B2500237.
方鑫,王云,龙贞莉等.工程菌,Clostridium butyricum-pMTL007-GLP-1通过PI3K/AKT/GSK-3β信号通路对A53T α-突触核蛋白小鼠模型的神经保护作用[J].浙江大学学报（英文版）（B辑：生物医学和生物技术）,2026,27(08):872-887. DOI： 10.1631/jzus.B2500237.

Xin FANG, Yun WANG, Zhenli LONG, et al. Neuroprotection of engineered Clostridium butyricum-pMTL007-GLP-1 in A53T α-synuclein (α-syn) mouse model via PI3K/AKT/GSK-3β[J]. Journal of Zhejiang University-SCIENCE B, 2026, 27(8): 872-887. DOI: 10.1631/jzus.B2500237. DOI：

摘要

帕金森病（PD）属于常见的神经退行性疾病，现有治疗手段有限且无法根治，亟需开发新型治疗方法。前期研究发现工程菌

Clostridium butyricum

-pMTL007-GLP-1（

C. butyricum

-pMTL007-GLP-1）可通过增强线粒体自噬改善PD症状，但具体分子机制未完全阐明。本研究通过进一步采用A53T α-突触核蛋白转基因PD小鼠模型，系统评估该工程菌株对运动功能、肠道α-突触核蛋白表达、肠屏障功能、肠道菌群结构及神经病理改变的影响，并重点探究PI3K/AKT/GSK-3β信号通路的作用机制。研究发现，

C. butyricum

-pMTL007-GLP-1可通过减少肠道α-突触核蛋白沉积、修复肠屏障功能及调节菌群多样性（尤其提高普雷沃菌属相对丰度）显著改善PD小鼠运动功能障碍。此外，该工程菌还可降低黑质区磷酸化α-突触核蛋白（p-α-syn）的水平，同时上调酪氨酸羟化酶（TH）、多巴胺转运体（DAT）和胰高血糖素样肽-1受体（GLP-1R）的表达，以减轻神经病理损伤。上述神经保护作用与抑制促炎反应、增强抗炎及抗凋亡信号传导相关，其机制可能通过激活PI3K/AKT/GSK-3β通路实现。综上，

C. butyricum

-pMTL007-GLP-1可通过重塑肠道菌群结构并激活PI3K/AKT/GSK-3β通路发挥显著的神经保护作用，从而为益生菌疗法应用于PD治疗提供了进一步的理论依据。

Abstract

Parkinson’s disease (PD) is a prevalent neurodegenerative disorder with limited therapeutic options and no cure

underscoring the urgent need for novel treatment strategies. Our previous work demonstrated that an engineered strain of

Clostridium butyricum

-pMTL007-glucagon-like peptide-1 (

C. butyricum

-pMTL007-GLP-1) alleviated PD symptoms by enhancing mitophagy

though the exact molecular mechanisms remained incompletely understood. In this study

we further investigated the neuroprotective effects and underlying mechanisms of this engineered strain using an A53T α-synuclein (α-syn) transgenic mouse model of PD. Specifically

we evaluated its impact on motor function

gut α-syn expression

intestinal barrier function

gut microbial composition

and neuropathological changes

with a focus on the phosphoinositide-3-kinase (PI3

K)/protein kinase B (AKT)/glycogen synthase kinase-3β (GSK-3β) signaling pathway. Our findings revealed that

C. butyricum

-pMTL007-GLP-1 ameliorated motor deficits in PD mice by reducing intestinal α-syn accumulation

restoring gut barrier function

and modulating microbial diversity—notably increasing the relative abundance of

Prevotella

at the genus level. Furthermore

the engineered strain attenuated neuropathological alterations by decreasing phosphorylated α-syn (p-α-syn) in the substantia nigra while upregulating tyrosine hydroxylase (TH)

dopamine-transporter (DAT)

and glucagon-like peptide-1-receptor (GLP-1R) expression. These neuroprotective effects were associated with suppressed proinflammatory responses and enhanced anti-inflammatory and anti-apoptotic signaling

likely mediated through PI3K/AKT/GSK-3β pathway activation. In conclusions

C. butyricum

-pMTL007-GLP-1 exerts significant neuroprotective effects in PD mice by reshaping gut microbiota composition and activating the PI3K/AKT/GSK-3β pathway. These findings provide further theoretical support for the potential application of probiotic-based therapies in PD treatment.

关键词

Keywords

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工程菌Clostridium butyricum-pMTL007-GLP-1通过PI3K/AKT/GSK-3β信号通路对A53T α-突触核蛋白小鼠模型的神经保护作用

Neuroprotection of engineered Clostridium butyricum-pMTL007-GLP-1 in A53T α-synuclein (α-syn) mouse model via PI3K/AKT/GSK-3β

DOI：10.1631/jzus.B2500237

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