The composition of the intestinal flora of patients with Parkinson's disease (PD) can change. However, whether reshaping the gut microbial composition can treat PD remains to be seen. The present study evaluated the effect of intestinal flora in the treatment of PD in a C57BL/6 mouse PD model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Chronic, low-dose, MPTP-treated mice exhibited upregulated gene expression levels of TNF-α and IL-1β in the substantia nigra (SN) of the mice, and induced intestinal microbial disorders. This indicated that the chronic low-dose MPTP model could be used to evaluate the progress of early intestinal pathology and intestinal flora imbalance in PD. After transplantation of faecal bacteria to MPTP-induced PD mice, the level of inflammation in the SN of the mice was reduced, and motor dysfunction was alleviated. Notably, faecal microbiota transplantation (FMT) upregulated the abundance of
Blautia
but downregulated
Anaerostipes
,
Bifidobacterium
,
ASF356
and
Ruminococcus
in the gut of PD mice. In addition, FMT reduced the activation of microglia and astrocytes in the SN and reduced the expression levels of GSK3β, IL-1β, inducible nitric oxide synthase and phosphorylated PTEN in the SN. Overall, the present study demonstrated that gut microbial dysfunction is associated with the pathogenesis of PD, and that FMT can protect PD mice by inhibiting neuroinflammation.
Ischemic stroke (CIS) is characterized by a high incidence, disability, and mortality. Numerous studies have demonstrated that intracranial arterial stenosis is an important pathological basis of CIS, and its main cause is atherosclerosis. Dyslipidemia is an important risk factor for atherosclerosis. Lysophosphatidic acid (Lpa), apolipoprotein -A(APO-A), and apolipoprotein -B(APO-B) proved to be significantly correlated with the severity of coronary artery disease. This study retrospectively collected the case data of 186 patients with CIS treated from May 2020 to May 2022 and explored the correlation between Lpa, APO-A, APO-B, and middle cerebral artery (MCA) stenosis in CIS patients.
The present study aimed to evaluate the effect of aerobic exercise training (AET) on the performance of mice with Parkinson's disease (PD) and to explore the molecular mechanism of AET-associated long noncoding RNAs (lncRNAs) in PD treatment. The results showed that the behaviors of PD mice were significantly improved after 4 weeks of AET. The substantia nigra pars compacta of PD mice showed scattered large multipolar cells and surrounding neutrophils after AET. In addition, a total of 62 differentially expressed lncRNAs (DE-lncRNAs) were identified between the AET group and the PD group, including 55 up-regulated and 7 down-regulated DE-lncRNAs in the AET group. Furthermore, the target genes of DE-lncRNAs, including LOC102633466, LOC102637865, and LOC102638670, were mainly involved in ECM-receptor interaction, the Wnt pathway and the PI3K/AKT/mTOR pathway. Quantitative real-time polymerase chain reaction showed that these three DE-lncRNAs were significantly up-regulated in the AET group than in the PD group. The lncRNA-miRNA-mRNA ceRNA network suggested that these 3 DE-lncRNAs may improve PD via the ceRNA mechanism. In conclusion, this study suggests that aerobic exercise improves motor performance of PD mice and provides a foundation for further studies on the molecular mechanism of lncRNAs in treating PD.
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