Dataset Information

Acupuncture Effect Assessment in APP/PS1 Transgenic Mice: On Regulating Learning-Memory Abilities, Gut Microbiota, and Microbial Metabolites.

ABSTRACT: Alzheimer's disease (AD) is a brain illness that affects learning and memory capacities over time. In recent investigations, acupuncture has been shown to be an effective alternative treatment for AD. We investigated the effect of acupuncture on learning and memory abilities using a water maze in APP/PS1 transgenic mice. The amounts of Aβ and tau protein in mice's hippocampal tissue were determined using Western blot. The levels of IL-1β, IL-10, LPS and TNF-α in mice's serum were measured using ELISA. The variations of gut microbiota in mice's feces were determined using the 16SrDNA technique, and the metabolites were examined using a untargeted metabolomics methodology. The results showed that acupuncture treatment improved mice's learning and memory abilities substantially. Acupuncture therapy regulated the Aβ and tau protein concentration as well as the levels of IL-10 and LPS. Acupuncture treatment influenced the mouse microbiota and metabolites and had been linked to six biochemical pathways. This study adds to our understanding of the effect of acupuncture on AD and opens the door to further research into the alterations of intestinal bacteria in the presence of AD.

SUBMITTER: Yang B

PROVIDER: S-EPMC9012623 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Acupuncture Effect Assessment in APP/PS1 Transgenic Mice: On Regulating Learning-Memory Abilities, Gut Microbiota, and Microbial Metabolites.

Yang Bo B He Min M Chen Xinhua X Sun Mengmeng M Pan Ting T Xu Xiaohong X Zhang Xuesong X Gong Qing Q Zhao Ye Y Jin Ziqi Z Cheng Zedong Z

Computational and mathematical methods in medicine 20220408

Alzheimer's disease (AD) is a brain illness that affects learning and memory capacities over time. In recent investigations, acupuncture has been shown to be an effective alternative treatment for AD. We investigated the effect of acupuncture on learning and memory abilities using a water maze in APP/PS1 transgenic mice. The amounts of Aβ and tau protein in mice's hippocampal tissue were determined using Western blot. The levels of IL-1β, IL-10, LPS and TNF-α in mice's serum ...[more]

PMID: 35432583

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Project description:Background: To explore the effect and mechanisms of Pantao Pill (PTP) on cognitive impairment. Methods: Network pharmacology was performed to analyze the mechanism of PTP treating cognitive impairment. The targets of PTP and cognitive impairment were predicted and used to construct protein-protein interaction (PPI) networks. The intersection network was selected, and the core network was obtained through topological analysis. Enrichment analysis was conducted to obtain the GOBP terms and KEGG pathways. We then performed experiments to validate the results of the network pharmacology by using an APP/PS1 transgenic mouse model. The APP/PS1 mice were divided into four groups: the model group, the high-dose PTP (3.6 g/kg·d) group, the low-dose PTP (1.8 g/kg·d) group, and the positive control group (donepezil hydrochloride, 2 mg/kg·d). Wild-type (WT) C57 mice served as a normal control group. PTP and donepezil were administered by gavage for 8 weeks. Results: Network pharmacology showed that PTP might improve cognitive impairment by regulating autophagy, apoptosis, and oxidative stress. For the Morris water maze test, a significant difference was shown in the total swimming distance among groups (p < 0.05) in the positioning navigation experiment, and with training time extension, the swimming speed increased (p < 0.01). In the space probe test, PTP administration significantly reduced the swimming path length and the escape latency of APP/PS1 mice (p < 0.05 or p < 0.01), whereas it had no effect on the swimming speed (p > 0.05). PTP (3.6 g/kg/d) rescued the reduction of norepinephrine and acetylcholine levels (p < 0.05), and increased the acetylcholinesterase concentration (p < 0.05) in the brain tissue. PTP (1.8 g/kg/d) increased the norepinephrine level (p < 0.01). PTP rescued the activity reduction of superoxide dismutase in the brain tissue (p < 0.01) and the neuron cell pyknosis in the hippocampal CA region (p < 0.05). PTP reduced ATG12 and PS1 expression (p < 0.05 or p < 0.01), and increased Bcl-2 expression in the brain tissue (p < 0.05). Conclusion: PTP can significantly improve the learning and memory abilities of APP/PS1 mice, and the mechanism may be related to the increase of neurotransmitter acetylcholine and norepinephrine levels, the reduction of the excessive autophagic activation, and the suppression of oxidative stress and excessive apoptotic activity.

Project description:Background: Fasudil, a Rho kinase inhibitor, exerts therapeutic effects in a mouse model of Alzheimer's disease (AD), a chronic neurodegenerative disease with progressive loss of memory. However, the mechanisms remain unclear. In addition, the gut microbiota and its metabolites have been implicated in AD. Methods: We examined the effect of fasudil on learning and memory using the Morris water-maze (MWM) test in APPswe/PSEN1dE9 transgenic (APP/PS1) mice (8 months old) treated (i.p.) with fasudil (25 mg/kg/day; ADF) or saline (ADNS) and in age- and gender-matched wild-type (WT) mice. Fecal metagenomics and metabolites were performed to identify novel biomarkers of AD and elucidate the mechanisms of fasudil induced beneficial effects in AD mice. Results: The MWM test showed significant improvement of spatial memory in APP/PS1 mice treated with fasudil as compared to ADNS. The metagenomic analysis revealed the abundance of the dominant phyla in all the three groups, including Bacteroidetes (23.7-44%) and Firmicutes (6.4-26.6%), and the increased relative abundance ratio of Firmicutes/Bacteroidetes in ADNS (59.1%) compared to WT (31.7%). In contrast, the Firmicutes/Bacteroidetes ratio was decreased to the WT level in ADF (32.8%). Lefse analysis of metagenomics identified s_Prevotella_sp_CAG873 as an ADF potential biomarker, while s_Helicobacter_typhlonius and s_Helicobacter_sp_MIT_03-1616 as ADNS potential biomarkers. Metabolite analysis revealed the increment of various metabolites, including glutamate, hypoxanthine, thymine, hexanoyl-CoA, and leukotriene, which were relative to ADNS or ADF microbiota potential biomarkers and mainly involved in the metabolism of nucleotide, lipids and sugars, and the inflammatory pathway. Conclusions: Memory deficit in APP/PS1 mice was correlated with the gut microbiome and metabolite status. Fasudil reversed the abnormal gut microbiota and subsequently regulated the related metabolisms to normal in the AD mice. It is believed that fasudil can be a novel strategy for the treatment of AD via remodeling of the gut microbiota and metabolites. The novel results also provide valuable references for the use of gut microbiota and metabolites as diagnostic biomarkers and/or therapeutic targets in clinical studies of AD.

Dataset Information

Acupuncture Effect Assessment in APP/PS1 Transgenic Mice: On Regulating Learning-Memory Abilities, Gut Microbiota, and Microbial Metabolites.

Publications

Acupuncture Effect Assessment in APP/PS1 Transgenic Mice: On Regulating Learning-Memory Abilities, Gut Microbiota, and Microbial Metabolites.

Similar Datasets

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