Post-ischemic protein restriction induces sustained neuroprotection, neurological recovery, brain remodeling, and gut microbiota rebalancing.


Journal

Brain, behavior, and immunity
ISSN: 1090-2139
Titre abrégé: Brain Behav Immun
Pays: Netherlands
ID NLM: 8800478

Informations de publication

Date de publication:
02 2022
Historique:
received: 11 05 2021
revised: 26 10 2021
accepted: 22 11 2021
pubmed: 2 12 2021
medline: 15 3 2022
entrez: 1 12 2021
Statut: ppublish

Résumé

Moderate dietary protein restriction confers neuroprotection when applied before ischemic stroke. How a moderately protein-reduced diet influences stroke recovery when administered after stroke, is a clinically relevant question. This question has not yet been investigated. Male C57BL6/J mice were exposed to transient intraluminal middle cerebral artery occlusion. Immediately after the stroke, mice were randomized to two normocaloric diets: a moderately protein-reduced diet containing 8% protein (PRD) or normal diet containing 20% protein (ND). Post-stroke neurological deficits were evaluated by a comprehensive test battery. Antioxidant and neuroinflammatory responses in the brain and liver were evaluated by Western blot and RTqPCR. Stroke-induced brain injury, microvascular integrity, glial responses, and neuroplasticity were assessed by immunohistochemistry. Fecal microbiota analysis was performed using 16S ribosomal RNA amplicon sequencing. We show that PRD reduces brain infarct volume after three days and enhances neurological and, specifically, motor-coordination recovery over six weeks in stroke mice. The recovery-promoting effects of PRD were associated with increased antioxidant responses and reduced neuroinflammation. Histochemical studies revealed that PRD increased long-term neuronal survival, increased peri-infarct microvascular density, reduced microglia/macrophage accumulation, increased contralesional pyramidal tract plasticity, and reduced brain atrophy. Fecal microbiota analysis showed reduced bacterial richness and diversity in ischemic mice on ND starting at 7 dpi. PRD restored bacterial richness and diversity at these time points. Moderate dietary protein restriction initiated post-ischemic stroke induces neurological recovery, brain remodeling, and neuroplasticity in mice by mechanisms involving antiinflammation and, in the post-acute phase, commensal gut microbiota rebalancing.

Sections du résumé

BACKGROUND
Moderate dietary protein restriction confers neuroprotection when applied before ischemic stroke. How a moderately protein-reduced diet influences stroke recovery when administered after stroke, is a clinically relevant question. This question has not yet been investigated.
METHODS
Male C57BL6/J mice were exposed to transient intraluminal middle cerebral artery occlusion. Immediately after the stroke, mice were randomized to two normocaloric diets: a moderately protein-reduced diet containing 8% protein (PRD) or normal diet containing 20% protein (ND). Post-stroke neurological deficits were evaluated by a comprehensive test battery. Antioxidant and neuroinflammatory responses in the brain and liver were evaluated by Western blot and RTqPCR. Stroke-induced brain injury, microvascular integrity, glial responses, and neuroplasticity were assessed by immunohistochemistry. Fecal microbiota analysis was performed using 16S ribosomal RNA amplicon sequencing.
RESULTS
We show that PRD reduces brain infarct volume after three days and enhances neurological and, specifically, motor-coordination recovery over six weeks in stroke mice. The recovery-promoting effects of PRD were associated with increased antioxidant responses and reduced neuroinflammation. Histochemical studies revealed that PRD increased long-term neuronal survival, increased peri-infarct microvascular density, reduced microglia/macrophage accumulation, increased contralesional pyramidal tract plasticity, and reduced brain atrophy. Fecal microbiota analysis showed reduced bacterial richness and diversity in ischemic mice on ND starting at 7 dpi. PRD restored bacterial richness and diversity at these time points.
CONCLUSION
Moderate dietary protein restriction initiated post-ischemic stroke induces neurological recovery, brain remodeling, and neuroplasticity in mice by mechanisms involving antiinflammation and, in the post-acute phase, commensal gut microbiota rebalancing.

Identifiants

pubmed: 34848338
pii: S0889-1591(21)00612-7
doi: 10.1016/j.bbi.2021.11.016
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

134-144

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.

Auteurs

Tayana Silva de Carvalho (T)

Department of Neurology, University Hospital Essen, Essen, Germany; Center for Translational and Behavioral Neurosciences, University Hospital Essen, Essen, Germany.

Vikramjeet Singh (V)

Institute for Experimental Immunology and Imaging, University Hospital Essen, Essen, Germany.

Ayan Mohamud Yusuf (A)

Department of Neurology, University Hospital Essen, Essen, Germany; Center for Translational and Behavioral Neurosciences, University Hospital Essen, Essen, Germany.

Jing Wang (J)

Department of Neurology, University Hospital Essen, Essen, Germany; Center for Translational and Behavioral Neurosciences, University Hospital Essen, Essen, Germany.

Adriana R Schultz Moreira (AR)

Department of Neurology, University Hospital Essen, Essen, Germany; Center for Translational and Behavioral Neurosciences, University Hospital Essen, Essen, Germany.

Eduardo H Sanchez-Mendoza (EH)

Department of Neurology, University Hospital Essen, Essen, Germany; Center for Translational and Behavioral Neurosciences, University Hospital Essen, Essen, Germany.

Maryam Sardari (M)

Department of Neurology, University Hospital Essen, Essen, Germany; Center for Translational and Behavioral Neurosciences, University Hospital Essen, Essen, Germany; Department of Animal Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran.

Luiza M Nascentes Melo (LM)

Department of Neurology, University Hospital Essen, Essen, Germany; Center for Translational and Behavioral Neurosciences, University Hospital Essen, Essen, Germany.

Thorsten R Doeppner (TR)

Department of Neurology, University Medicine Göttingen, Göttingen, Germany.

Jan Kehrmann (J)

Institute of Medical Microbiology, University Hospital Essen, Essen, Germany.

Rene Scholtysik (R)

Institute of Cell Biology, University Hospital Essen, Essen, Germany.

Ludger Hitpass (L)

Institute of Cell Biology, University Hospital Essen, Essen, Germany.

Matthias Gunzer (M)

Institute for Experimental Immunology and Imaging, University Hospital Essen, Essen, Germany; Leibniz-Institut für Analytische Wissenschaften ISAS e.V, Dortmund, Germany.

Dirk M Hermann (DM)

Department of Neurology, University Hospital Essen, Essen, Germany; Center for Translational and Behavioral Neurosciences, University Hospital Essen, Essen, Germany. Electronic address: dirk.hermann@uk-essen.de.

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