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胃感染部分保护 6-OHDA 帕金森病小鼠模型中的神经毒性。

Gastric Infection Partially Protects against Neurotoxicity in A 6-OHDA Parkinson's Disease Mouse Model.

机构信息

Department of Pathobiology, Pharmacology and Zoological Medicine, Faculty of Veterinary Medicine, Ghent University, 9820 Merelbeke, Belgium.

VIB Center for Inflammation Research, 9052 Ghent, Belgium.

出版信息

Int J Mol Sci. 2021 Oct 20;22(21):11328. doi: 10.3390/ijms222111328.

DOI:10.3390/ijms222111328
PMID:34768765
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8582972/
Abstract

The exact etiology of Parkinson's disease (PD) remains largely unknown, but more and more research suggests the involvement of the gut microbiota. Interestingly, idiopathic PD patients were shown to have at least a 10 times higher prevalence of () DNA in gastric biopsies compared to control patients. is a zoonotic species that naturally colonizes the stomach of pigs and non-human primates but can be transmitted to humans. Here, we investigated the influence of a gastric infection on PD disease progression through a 6-hydroxydopamine (6-OHDA) mouse model. Therefore, mice with either a short- or long-term infection were stereotactically injected with 6-OHDA in the left striatum and sampled one week later. Remarkably, a reduced loss of dopaminergic neurons was seen in the 6-OHDA groups compared to the control/6-OHDA groups. Correspondingly, motor function of the -infected 6-OHDA mice was superior to that in the non-infected 6-OHDA mice. Interestingly, we also observed higher expression levels of antioxidant genes in brain tissue from -infected 6-OHDA mice, as a potential explanation for the reduced 6-OHDA-induced cell loss. Our data support an unexpected neuroprotective effect of gastric on PD pathology, mediated through changes in oxidative stress.

摘要

帕金森病（PD）的确切病因在很大程度上尚不清楚，但越来越多的研究表明肠道微生物群的参与。有趣的是，与对照组患者相比，特发性 PD 患者的胃活检中至少有 10 倍更高的（）DNA 患病率。是一种人畜共患的物种，它自然定植在猪和非人类灵长类动物的胃中，但可以传播给人类。在这里，我们通过 6-羟多巴胺（6-OHDA）小鼠模型研究了胃（）感染对 PD 疾病进展的影响。因此，将短期或长期（）感染的小鼠立体定向注射到左侧纹状体中的 6-OHDA 中，并在一周后取样。值得注意的是，与对照组/6-OHDA 组相比，6-OHDA 组中多巴胺能神经元的丢失减少。相应地，感染（）的 6-OHDA 小鼠的运动功能优于未感染的 6-OHDA 小鼠。有趣的是，我们还观察到感染（）的 6-OHDA 小鼠脑组织中抗氧化基因的表达水平更高，这可能是减少 6-OHDA 诱导的细胞丢失的潜在解释。我们的数据支持胃（）对 PD 病理的意外神经保护作用，这是通过氧化应激的变化介导的。

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