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Related Experiment Video

Updated: May 17, 2026

Isolation of Region-specific Microglia from One Adult Mouse Brain Hemisphere for Deep Single-cell RNA Sequencing

Isolation of Region-specific Microglia from One Adult Mouse Brain Hemisphere for Deep Single-cell RNA Sequencing

Published on: December 3, 2019

Single-Cell RNA-Seq Revealed the Immune Microenvironment Reprogramming by Dexmedetomidine Treatment in Ischemic

Wenyi Zhang^1,2, Xingyun Wang^1,3, Bing Zhang¹

¹Department of Anesthesiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200336, China.

Molecular Neurobiology

|August 1, 2025

Summary

Dexmedetomidine (DEX) reduces stroke damage by preserving microglial function through metabolic regulation. This study identifies HK2 as key to DEX

Keywords:

Apoptosis Dexmedetomidine MCAO ScRNA-seq Stroke

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Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

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Last Updated: May 17, 2026

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Published on: December 3, 2019

Preparation of a Non-Cardiomyocyte Cell Suspension for Single-Cell RNA Sequencing from a Post-Myocardial Infarction Adult Mouse Heart

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Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Area of Science:

Neuroscience
Immunology
Metabolomics

Background:

Dexmedetomidine (DEX) shows neuroprotective effects in cerebral ischemia.
The precise mechanisms underlying DEX's protective actions are not fully understood.

Purpose of the Study:

To elucidate the mechanisms of DEX's neuroprotection in cerebral ischemia.
To investigate DEX's impact on microglial function and immune response.

Main Methods:

Multi-omics approaches including RNA-seq, metabolomics, and single-cell RNA-seq.
Middle cerebral artery occlusion (MCAO) mouse model for cerebral ischemia.
Validation in oxygen-glucose deprivation models.

Main Results:

DEX pretreatment reduced infarct volume and improved neurological function in MCAO mice.
DEX preserved microglial phagocytic function via metabolic regulation, decreasing apoptosis.
DEX attenuated immune dysregulation by reducing neutrophils, B cells, and antigen-presenting fibroblasts.
HK2 (hexokinase 2) was identified as a key regulator of microglial homeostasis and inflammation.

Conclusions:

DEX protects against cerebral ischemia-reperfusion injury by maintaining immune microenvironment homeostasis.
Microglial metabolic reprogramming mediated by HK2 is a key mechanism for DEX's neuroprotection.
These findings support the translational potential of DEX in ischemic stroke therapy.