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CCFM1067 对 MPTP 诱导的帕金森病小鼠模型的神经保护作用。

Neuroprotective Effects of CCFM1067 in MPTP-Induced Mouse Models of Parkinson's Disease.

机构信息

State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.

School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.

出版信息

Nutrients. 2022 Nov 4;14(21):4678. doi: 10.3390/nu14214678.

DOI:10.3390/nu14214678
PMID:36364939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9655354/
Abstract

There is mounting evidence that the microbiota-gut-brain axis (MGBA) is critical in the pathogenesis and progression of Parkinson's disease (PD), suggesting that probiotic therapy restoring gut microecology may slow down disease progression. In this study, we examined the disease-alleviating effects of CCFM1067, orally administered for 5 weeks in a PD mouse model. Our study shows that supplementation with the probiotic CCFM1067 protected dopaminergic neurons and suppressed glial cell hyperactivation and neuroinflammation in PD mice. In addition, the antioxidant capacity of the central nervous system was enhanced and oxidative stress was alleviated. Moreover, CCFM1067 protected the blood-brain and intestinal barriers from damage in the MPTP-induced mouse model. The results of fecal microbiota analysis showed that CCFM1067 intervention could act on the MPTP-induced microecological imbalance in the intestinal microbiota, suppressing the number of pathogenic bacteria () while increasing the number of beneficial bacteria ( and ) in PD mice. In addition, the increase in short chain fatty acids (acetic and butyric acids) may explain the anti-inflammatory action of CCFM1067 in the gut or brain of the MPTP-induced PD mouse model. In conclusion, we demonstrated that the probiotic CCFM1067, which can prevent or treat PD by modulating the gut-brain axis, can be utilized as a possible new oral supplement for PD therapy.

摘要

越来越多的证据表明,微生物群-肠道-大脑轴(MGBA)在帕金森病(PD)的发病机制和进展中至关重要,这表明恢复肠道微生物群的益生菌疗法可能会减缓疾病进展。在这项研究中,我们研究了 CCFM1067 在 PD 小鼠模型中口服给药 5 周的疾病缓解作用。我们的研究表明,补充益生菌 CCFM1067 可保护多巴胺能神经元,并抑制 PD 小鼠中的神经胶质细胞过度激活和神经炎症。此外,中枢神经系统的抗氧化能力增强,氧化应激减轻。此外,CCFM1067 可保护血脑和肠道屏障免受 MPTP 诱导的小鼠模型的损伤。粪便微生物组分析的结果表明,CCFM1067 干预可以作用于 MPTP 诱导的肠道微生物组的微生态失衡,抑制致病性细菌()的数量,同时增加 PD 小鼠中有益细菌(和)的数量。此外,短链脂肪酸(乙酸和丁酸)的增加可能解释了 CCFM1067 在 MPTP 诱导的 PD 小鼠模型的肠道或大脑中的抗炎作用。总之,我们证明了益生菌 CCFM1067 可以通过调节肠道-大脑轴来预防或治疗 PD,可以作为 PD 治疗的一种潜在新的口服补充剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c46f/9655354/dc13d708c514/nutrients-14-04678-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c46f/9655354/ef1ca8776e79/nutrients-14-04678-g002.jpg
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