Related Experiment Video
Updated: Aug 16, 2025

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
Published on: June 10, 2020
Inflammatory role of microglia in brain injury caused by subarachnoid hemorrhage
Xiao-Yi Wang1, Fan Wu1, Ren-Ya Zhan1
1Department of Neurosurgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Abstract:
Early brain injury is a series of pathophysiological changes and direct damage of brain tissue within 72 h after subarachnoid hemorrhage before cerebral vasospasm occurs. Early brain injury is a key factor affecting the prognosis of subarachnoid hemorrhage, and its possible pathological mechanisms include oxidative stress, cell apoptosis, autophagy, and immune inflammation. Microglia are important immune cells of the central nervous system. Microglia play a dual role in protection and injury. Microglia are involved in the occurrence of brain edema, the processes of neuronal apoptosis, and the blood-brain barrier disruption after subarachnoid hemorrhage (SAH) through the signaling pathways mediated by receptors such as Toll-like receptor 4 (TLR4), calcium-sensing receptor (CaSR), and triggering receptor expressed on myeloid cells-1 (TREM-1), which secrete pro-inflammatory cytokines such as interleukins and tumor necrosis factor α. Conversely, they exert their anti-inflammatory and protective effects by expressing substances such as neuroglobin and heme oxygenase-1. This article reviews the latest developments in single-cell transcriptomics for microglia in early brain injury after subarachnoid hemorrhage and its inflammatory role.
Insights
Early brain injury after subarachnoid hemorrhage involves complex inflammation. Single-cell transcriptomics reveals microglia
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Early brain injury (EBI) following subarachnoid hemorrhage (SAH) significantly impacts patient prognosis.
- EBI involves oxidative stress, apoptosis, autophagy, and neuroinflammation.
- Microglia, the brain's immune cells, play a critical dual role in EBI, contributing to both damage and protection.
Purpose of the Study:
- To review the application of single-cell transcriptomics in understanding microglia's role in EBI after SAH.
- To elucidate the inflammatory mechanisms mediated by microglia in the early stages of SAH.
Main Methods:
- Review of current literature on single-cell transcriptomics.
- Analysis of microglia-mediated signaling pathways (TLR4, CaSR, TREM-1) in SAH.
- Examination of pro-inflammatory and anti-inflammatory mediators released by microglia.
Main Results:
- Single-cell transcriptomics provides high-resolution insights into microglial heterogeneity and function in EBI.
- Microglia contribute to brain edema, neuronal apoptosis, and blood-brain barrier disruption via specific receptor pathways.
- Microglia also exert protective effects through the expression of neuroglobin and heme oxygenase-1.
Conclusions:
- Microglia exhibit complex and context-dependent roles in early brain injury after subarachnoid hemorrhage.
- Single-cell transcriptomics is a powerful tool for dissecting these roles and identifying therapeutic targets.
- Further research is needed to fully harness microglia's potential for improving SAH outcomes.

