Gut microbiota is closely related to the Parkinson's disease (PD) pathogenesis. Additionally, aggregation of α-synuclein (α-syn) is central to PD pathogenesis. Here we identified the further mechanisms of gut microbiota in PD. A mouse model with PD was established via injection of MPTP. Normal or MPTP-induced PD like animals were treated with FMT from healthy normal mice. Pole test and traction test were performed to examine the effects of FMT on motor function of PD mice. Fecal SCFAs were assessed by gas chromatography-mass spectrometry. The α-syn level in the substantia nigra pars compacta (SN) of mice was measured using western blot. Dopaminergic neurons and microglial activation in the SN were analyzed by immunohistochemistry (IHC) and immunofluorescence (IF) staining. FMT alleviated physical impairment, decreased fecal SCFAs in a mouse model of PD. Additionally, FMT decreased the expression of α-syn, as well as inhibited the activation of microglia in the SN, and blocked the TLR4/PI3K/AKT/NF-κB signaling in the SN and striatum. FMT could protect mice against PD via suppressing α-syn expression and inactivating the TLR4/PI3K/AKT/NF-κB signaling.

中文翻译：

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粪便微生物群移植通过 α-突触核蛋白刺激的 TLR4/PI3K/AKT/NF-κB 通路在 MPTP 诱导的帕金森病中发挥保护作用。

肠道菌群与帕金森病 (PD) 的发病机制密切相关。此外，α-突触核蛋白 (α-syn) 的聚集是 PD 发病机制的核心。在这里，我们确定了 PD 中肠道微生物群的进一步机制。通过注射MPTP建立PD小鼠模型。用来自健康正常小鼠的 FMT 治疗正常或 MPTP 诱导的 PD 样动物。进行了极点试验和牵引试验，以检查FMT对PD小鼠运动功能的影响。通过气相色谱-质谱法评估粪便 SCFA。使用蛋白质印迹测量小鼠黑质致密部（SN）中的α-syn水平。通过免疫组织化学 (IHC) 和免疫荧光 (IF) 染色分析 SN 中的多巴胺能神经元和小胶质细胞活化。FMT减轻了身体损伤，在 PD 小鼠模型中减少粪便 SCFA。此外，FMT 降低了 α-syn 的表达，抑制了 SN 中小胶质细胞的活化，并阻断了 SN 和纹状体中的 TLR4/PI3K/AKT/NF-κB 信号传导。FMT 可以通过抑制 α-syn 表达和使 TLR4/PI3K/AKT/NF-κB 信号失活来保护小鼠免受 PD。