Fecal microbiota transplantation and short‐chain fatty acids protected against cognitive dysfunction in a rat model of chronic cerebral hypoperfusion

Aims Clear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short‐chain fatty acids (SCFAs) alterations in chronic cerebral ischemic pathogenesis have yet to be explored. In this study, we investigated chronic cerebral hypoperfusion (CCH)‐induced gut microbiota an...

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Published inCNS neuroscience & therapeutics Vol. 29; no. S1; pp. 98 - 114
Main Authors Su, Shao‐Hua, Chen, Ming, Wu, Yi‐Fang, Lin, Qi, Wang, Da‐Peng, Sun, Jun, Hai, Jian
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.06.2023
John Wiley and Sons Inc
Subjects
Acetic acid
Alzheimer's disease
Animal cognition
Animals
Antibiotics
Brain Ischemia - therapy
Carotid arteries
Carotid artery
Cerebral blood flow
chronic cerebral hypoperfusion
Cognitive ability
cognitive dysfunction
Cognitive Dysfunction - etiology
Cognitive Dysfunction - therapy
Community structure
Discriminant analysis
Dysbacteriosis
Enzyme-linked immunosorbent assay
Fatty acids
Fatty Acids, Volatile - analysis
fecal microbiota transplantation
Fecal Microbiota Transplantation - methods
Fecal microflora
Feces
Feces - chemistry
Gas chromatography
Genetic testing
Hippocampus
Immunofluorescence
Immunoprecipitation
Inflammation
Intestinal microflora
Ischemia
Laboratory animals
Mass spectroscopy
Metabolism
Microbiota
Microglia
Original
Oxidative phosphorylation
Phenotypes
Phosphorylation
Propionic acid
Rats
rRNA 16S
short‐chain fatty acids
Sodium
Stroke
Synapses
synaptic plasticity
Transplantation
Veins & arteries
Vesicle fusion
United States > US
China
synaptic plasticity
short-chain fatty acids
chronic cerebral hypoperfusion
cognitive dysfunction
microglia
fecal microbiota transplantation
oxidative phosphorylation
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Abstract Aims Clear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short‐chain fatty acids (SCFAs) alterations in chronic cerebral ischemic pathogenesis have yet to be explored. In this study, we investigated chronic cerebral hypoperfusion (CCH)‐induced gut microbiota and metabolic profiles of SCFAs as well as the effects and mechanisms of fecal microbiota transplantation (FMT) and SCFAs treatment on CCH‐induced hippocampal neuronal injury. Methods Bilateral common carotid artery occlusion (BCCAo) was used to establish the CCH model. Gut microbiota and SCFAs profiles in feces and hippocampus were evaluated by 16S ribosomal RNA sequencing and gas chromatography–mass spectrometry. RNA sequencing analysis was performed in hippocampal tissues. The potential molecular pathways and differential genes were verified through western blot, immunoprecipitation, immunofluorescence, and ELISA. Cognitive function was assessed via the Morris water maze test. Ultrastructures of mitochondria and synapses were tested through a transmission electron microscope. Results Chronic cerebral hypoperfusion induced decreased fecal acetic and propionic acid and reduced hippocampal acetic acid, which were reversed after FMT and SCFAs administration by changing fecal microbial community structure and compositions. Furthermore, in the hippocampus, FMT and SCFAs replenishment exerted anti‐neuroinflammatory effects through inhibiting microglial and astrocytic activation as well as switching microglial phenotype from M1 toward M2. Moreover, FMT and SCFAs treatment alleviated neuronal loss and microglia‐mediated synaptic loss and maintained the normal process of synaptic vesicle fusion and release, resulting in the improvement of synaptic plasticity. In addition, FMT and SCFAs supplement prevented oxidative phosphorylation dysfunction via mitochondrial metabolic reprogramming. The above effects of FMT and SCFAs treatment led to the inhibition of CCH‐induced cognitive impairment. Conclusion Our findings highlight FMT and SCFAs replenishment would be the feasible gut microbiota‐based strategy to mitigate chronic cerebral ischemia‐induced neuronal injury. Fecal microbiota transplantation (FMT) and short‐chain fatty acids (SCFAs) replenishment exerted anti‐neuroinflammatory effects through switching microglial phenotype from M1 toward M2. Furthermore, FMT and SCFAs treatment alleviated neuronal loss and microglia‐mediated synaptic loss and maintained the normal process of synaptic vesicle fusion and release, resulting in the improvement of synaptic plasticity. In addition, FMT and SCFAs supplement prevented oxidative phosphorylation dysfunction via mitochondrial metabolic reprogramming.
AbstractList Fecal microbiota transplantation (FMT) and short‐chain fatty acids (SCFAs) replenishment exerted anti‐neuroinflammatory effects through switching microglial phenotype from M1 toward M2. Furthermore, FMT and SCFAs treatment alleviated neuronal loss and microglia‐mediated synaptic loss and maintained the normal process of synaptic vesicle fusion and release, resulting in the improvement of synaptic plasticity. In addition, FMT and SCFAs supplement prevented oxidative phosphorylation dysfunction via mitochondrial metabolic reprogramming.
Clear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short-chain fatty acids (SCFAs) alterations in chronic cerebral ischemic pathogenesis have yet to be explored. In this study, we investigated chronic cerebral hypoperfusion (CCH)-induced gut microbiota and metabolic profiles of SCFAs as well as the effects and mechanisms of fecal microbiota transplantation (FMT) and SCFAs treatment on CCH-induced hippocampal neuronal injury. Bilateral common carotid artery occlusion (BCCAo) was used to establish the CCH model. Gut microbiota and SCFAs profiles in feces and hippocampus were evaluated by 16S ribosomal RNA sequencing and gas chromatography-mass spectrometry. RNA sequencing analysis was performed in hippocampal tissues. The potential molecular pathways and differential genes were verified through western blot, immunoprecipitation, immunofluorescence, and ELISA. Cognitive function was assessed via the Morris water maze test. Ultrastructures of mitochondria and synapses were tested through a transmission electron microscope. Chronic cerebral hypoperfusion induced decreased fecal acetic and propionic acid and reduced hippocampal acetic acid, which were reversed after FMT and SCFAs administration by changing fecal microbial community structure and compositions. Furthermore, in the hippocampus, FMT and SCFAs replenishment exerted anti-neuroinflammatory effects through inhibiting microglial and astrocytic activation as well as switching microglial phenotype from M1 toward M2. Moreover, FMT and SCFAs treatment alleviated neuronal loss and microglia-mediated synaptic loss and maintained the normal process of synaptic vesicle fusion and release, resulting in the improvement of synaptic plasticity. In addition, FMT and SCFAs supplement prevented oxidative phosphorylation dysfunction via mitochondrial metabolic reprogramming. The above effects of FMT and SCFAs treatment led to the inhibition of CCH-induced cognitive impairment. Our findings highlight FMT and SCFAs replenishment would be the feasible gut microbiota-based strategy to mitigate chronic cerebral ischemia-induced neuronal injury.
AimsClear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short-chain fatty acids (SCFAs) alterations in chronic cerebral ischemic pathogenesis have yet to be explored. In this study, we investigated chronic cerebral hypoperfusion (CCH)-induced gut microbiota and metabolic profiles of SCFAs as well as the effects and mechanisms of fecal microbiota transplantation (FMT) and SCFAs treatment on CCH-induced hippocampal neuronal injury.MethodsBilateral common carotid artery occlusion (BCCAo) was used to establish the CCH model. Gut microbiota and SCFAs profiles in feces and hippocampus were evaluated by 16S ribosomal RNA sequencing and gas chromatography–mass spectrometry. RNA sequencing analysis was performed in hippocampal tissues. The potential molecular pathways and differential genes were verified through western blot, immunoprecipitation, immunofluorescence, and ELISA. Cognitive function was assessed via the Morris water maze test. Ultrastructures of mitochondria and synapses were tested through a transmission electron microscope.ResultsChronic cerebral hypoperfusion induced decreased fecal acetic and propionic acid and reduced hippocampal acetic acid, which were reversed after FMT and SCFAs administration by changing fecal microbial community structure and compositions. Furthermore, in the hippocampus, FMT and SCFAs replenishment exerted anti-neuroinflammatory effects through inhibiting microglial and astrocytic activation as well as switching microglial phenotype from M1 toward M2. Moreover, FMT and SCFAs treatment alleviated neuronal loss and microglia-mediated synaptic loss and maintained the normal process of synaptic vesicle fusion and release, resulting in the improvement of synaptic plasticity. In addition, FMT and SCFAs supplement prevented oxidative phosphorylation dysfunction via mitochondrial metabolic reprogramming. The above effects of FMT and SCFAs treatment led to the inhibition of CCH-induced cognitive impairment.ConclusionOur findings highlight FMT and SCFAs replenishment would be the feasible gut microbiota-based strategy to mitigate chronic cerebral ischemia-induced neuronal injury.
Aims Clear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short‐chain fatty acids (SCFAs) alterations in chronic cerebral ischemic pathogenesis have yet to be explored. In this study, we investigated chronic cerebral hypoperfusion (CCH)‐induced gut microbiota and metabolic profiles of SCFAs as well as the effects and mechanisms of fecal microbiota transplantation (FMT) and SCFAs treatment on CCH‐induced hippocampal neuronal injury. Methods Bilateral common carotid artery occlusion (BCCAo) was used to establish the CCH model. Gut microbiota and SCFAs profiles in feces and hippocampus were evaluated by 16S ribosomal RNA sequencing and gas chromatography–mass spectrometry. RNA sequencing analysis was performed in hippocampal tissues. The potential molecular pathways and differential genes were verified through western blot, immunoprecipitation, immunofluorescence, and ELISA. Cognitive function was assessed via the Morris water maze test. Ultrastructures of mitochondria and synapses were tested through a transmission electron microscope. Results Chronic cerebral hypoperfusion induced decreased fecal acetic and propionic acid and reduced hippocampal acetic acid, which were reversed after FMT and SCFAs administration by changing fecal microbial community structure and compositions. Furthermore, in the hippocampus, FMT and SCFAs replenishment exerted anti‐neuroinflammatory effects through inhibiting microglial and astrocytic activation as well as switching microglial phenotype from M1 toward M2. Moreover, FMT and SCFAs treatment alleviated neuronal loss and microglia‐mediated synaptic loss and maintained the normal process of synaptic vesicle fusion and release, resulting in the improvement of synaptic plasticity. In addition, FMT and SCFAs supplement prevented oxidative phosphorylation dysfunction via mitochondrial metabolic reprogramming. The above effects of FMT and SCFAs treatment led to the inhibition of CCH‐induced cognitive impairment. Conclusion Our findings highlight FMT and SCFAs replenishment would be the feasible gut microbiota‐based strategy to mitigate chronic cerebral ischemia‐induced neuronal injury. Fecal microbiota transplantation (FMT) and short‐chain fatty acids (SCFAs) replenishment exerted anti‐neuroinflammatory effects through switching microglial phenotype from M1 toward M2. Furthermore, FMT and SCFAs treatment alleviated neuronal loss and microglia‐mediated synaptic loss and maintained the normal process of synaptic vesicle fusion and release, resulting in the improvement of synaptic plasticity. In addition, FMT and SCFAs supplement prevented oxidative phosphorylation dysfunction via mitochondrial metabolic reprogramming.
Clear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short-chain fatty acids (SCFAs) alterations in chronic cerebral ischemic pathogenesis have yet to be explored. In this study, we investigated chronic cerebral hypoperfusion (CCH)-induced gut microbiota and metabolic profiles of SCFAs as well as the effects and mechanisms of fecal microbiota transplantation (FMT) and SCFAs treatment on CCH-induced hippocampal neuronal injury.AIMSClear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short-chain fatty acids (SCFAs) alterations in chronic cerebral ischemic pathogenesis have yet to be explored. In this study, we investigated chronic cerebral hypoperfusion (CCH)-induced gut microbiota and metabolic profiles of SCFAs as well as the effects and mechanisms of fecal microbiota transplantation (FMT) and SCFAs treatment on CCH-induced hippocampal neuronal injury.Bilateral common carotid artery occlusion (BCCAo) was used to establish the CCH model. Gut microbiota and SCFAs profiles in feces and hippocampus were evaluated by 16S ribosomal RNA sequencing and gas chromatography-mass spectrometry. RNA sequencing analysis was performed in hippocampal tissues. The potential molecular pathways and differential genes were verified through western blot, immunoprecipitation, immunofluorescence, and ELISA. Cognitive function was assessed via the Morris water maze test. Ultrastructures of mitochondria and synapses were tested through a transmission electron microscope.METHODSBilateral common carotid artery occlusion (BCCAo) was used to establish the CCH model. Gut microbiota and SCFAs profiles in feces and hippocampus were evaluated by 16S ribosomal RNA sequencing and gas chromatography-mass spectrometry. RNA sequencing analysis was performed in hippocampal tissues. The potential molecular pathways and differential genes were verified through western blot, immunoprecipitation, immunofluorescence, and ELISA. Cognitive function was assessed via the Morris water maze test. Ultrastructures of mitochondria and synapses were tested through a transmission electron microscope.Chronic cerebral hypoperfusion induced decreased fecal acetic and propionic acid and reduced hippocampal acetic acid, which were reversed after FMT and SCFAs administration by changing fecal microbial community structure and compositions. Furthermore, in the hippocampus, FMT and SCFAs replenishment exerted anti-neuroinflammatory effects through inhibiting microglial and astrocytic activation as well as switching microglial phenotype from M1 toward M2. Moreover, FMT and SCFAs treatment alleviated neuronal loss and microglia-mediated synaptic loss and maintained the normal process of synaptic vesicle fusion and release, resulting in the improvement of synaptic plasticity. In addition, FMT and SCFAs supplement prevented oxidative phosphorylation dysfunction via mitochondrial metabolic reprogramming. The above effects of FMT and SCFAs treatment led to the inhibition of CCH-induced cognitive impairment.RESULTSChronic cerebral hypoperfusion induced decreased fecal acetic and propionic acid and reduced hippocampal acetic acid, which were reversed after FMT and SCFAs administration by changing fecal microbial community structure and compositions. Furthermore, in the hippocampus, FMT and SCFAs replenishment exerted anti-neuroinflammatory effects through inhibiting microglial and astrocytic activation as well as switching microglial phenotype from M1 toward M2. Moreover, FMT and SCFAs treatment alleviated neuronal loss and microglia-mediated synaptic loss and maintained the normal process of synaptic vesicle fusion and release, resulting in the improvement of synaptic plasticity. In addition, FMT and SCFAs supplement prevented oxidative phosphorylation dysfunction via mitochondrial metabolic reprogramming. The above effects of FMT and SCFAs treatment led to the inhibition of CCH-induced cognitive impairment.Our findings highlight FMT and SCFAs replenishment would be the feasible gut microbiota-based strategy to mitigate chronic cerebral ischemia-induced neuronal injury.CONCLUSIONOur findings highlight FMT and SCFAs replenishment would be the feasible gut microbiota-based strategy to mitigate chronic cerebral ischemia-induced neuronal injury.
Author Chen, Ming
Lin, Qi
Su, Shao‐Hua
Sun, Jun
Hai, Jian
Wang, Da‐Peng
Wu, Yi‐Fang
AuthorAffiliation 2 Department of Neurosurgery, Xinhua hospital, School of Medicine Shanghai Jiao Tong University Shanghai China
3 Department of Pharmacy, Institutes of Medical Sciences, School of Medicine Shanghai Jiao Tong University Shanghai China
1 Department of Neurosurgery, Tongji Hospital, School of Medicine Tongji University Shanghai China
AuthorAffiliation_xml – name: 3 Department of Pharmacy, Institutes of Medical Sciences, School of Medicine Shanghai Jiao Tong University Shanghai China
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/36627762$$D View this record in MEDLINE/PubMed
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Tue Jul 01 00:33:49 EDT 2025
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Issue S1
Keywords synaptic plasticity
short-chain fatty acids
chronic cerebral hypoperfusion
cognitive dysfunction
microglia
fecal microbiota transplantation
oxidative phosphorylation
Language English
License Attribution
2023 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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Notes Shao‐Hua Su and Ming Chen contributed equally to this work.
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Snippet Aims Clear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short‐chain fatty acids (SCFAs) alterations in chronic cerebral...
Clear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short-chain fatty acids (SCFAs) alterations in chronic cerebral...
AimsClear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short-chain fatty acids (SCFAs) alterations in chronic cerebral...
Fecal microbiota transplantation (FMT) and short‐chain fatty acids (SCFAs) replenishment exerted anti‐neuroinflammatory effects through switching microglial...
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SourceType Open Access Repository
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StartPage 98
SubjectTerms Acetic acid
Alzheimer's disease
Animal cognition
Animals
Antibiotics
Brain Ischemia - therapy
Carotid arteries
Carotid artery
Cerebral blood flow
chronic cerebral hypoperfusion
Cognitive ability
cognitive dysfunction
Cognitive Dysfunction - etiology
Cognitive Dysfunction - therapy
Community structure
Discriminant analysis
Dysbacteriosis
Enzyme-linked immunosorbent assay
Fatty acids
Fatty Acids, Volatile - analysis
fecal microbiota transplantation
Fecal Microbiota Transplantation - methods
Fecal microflora
Feces
Feces - chemistry
Gas chromatography
Genetic testing
Hippocampus
Immunofluorescence
Immunoprecipitation
Inflammation
Intestinal microflora
Ischemia
Laboratory animals
Mass spectroscopy
Metabolism
Microbiota
Microglia
Original
Oxidative phosphorylation
Phenotypes
Phosphorylation
Propionic acid
Rats
rRNA 16S
short‐chain fatty acids
Sodium
Stroke
Synapses
synaptic plasticity
Transplantation
Veins & arteries
Vesicle fusion
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Title Fecal microbiota transplantation and short‐chain fatty acids protected against cognitive dysfunction in a rat model of chronic cerebral hypoperfusion
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fcns.14089
https://www.ncbi.nlm.nih.gov/pubmed/36627762
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Volume 29
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