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Updated: Jun 10, 2026

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
Published on: June 10, 2020
Preclinical and clinical research on inflammation after intracerebral hemorrhage
1Department of Anesthesiology/Critical Care Medicine, The Johns Hopkins University, School of Medicine, 720 Rutland Avenue, Traylor Building 809, Baltimore, MD 21205, USA. jwang79@jhmi.edu.
Insights
Intracerebral hemorrhage (ICH) involves inflammation, impacting secondary brain injury. Targeting neuroinflammation offers promising therapeutic strategies for this lethal stroke subtype.
Area of Science:
- Neurology
- Neuroscience
- Pathophysiology
Background:
- Intracerebral hemorrhage (ICH) is a severe stroke subtype with high mortality.
- ICH pathophysiology is less understood than ischemic stroke.
- Inflammatory mechanisms are implicated in secondary brain injury following ICH.
Purpose of the Study:
- To review recent progress in preclinical ICH models.
- To survey studies on inflammatory cells and mediators in ICH.
- To highlight potential therapeutic targets for ICH.
Main Methods:
- Review of preclinical and clinical studies on ICH.
- Analysis of research on inflammatory cells (microglia, macrophages, etc.).
- Survey of inflammatory mediators (MMPs, Nrf2, heme oxygenase, iron).
Main Results:
- Microglial activation occurs early in preclinical ICH models.
- Neuroinflammation plays a key role in ICH progression.
- Several molecular targets and therapeutic strategies have emerged.
Conclusions:
- Inflammatory mechanisms are central to ICH-induced secondary brain injury.
- Targeting neuroinflammation presents therapeutic promise for ICH.
- Further research into these pathways is crucial for developing effective treatments.
Abstract:
Intracerebral hemorrhage (ICH) is one of the most lethal stroke subtypes. Despite the high morbidity and mortality associated with ICH, its pathophysiology has not been investigated as well as that of ischemic stroke. Available evidence from preclinical and clinical studies suggests that inflammatory mechanisms are involved in the progression of ICH-induced secondary brain injury. For example, in preclinical ICH models, microglial activation has been shown to occur within 1h, much earlier than neutrophil infiltration. Recent advances in our understanding of neuroinflammatory pathways have revealed several new molecular targets, and related therapeutic strategies have been tested in preclinical ICH models. This review summarizes recent progress made in preclinical models of ICH, surveys preclinical and clinical studies of inflammatory cells (leukocytes, macrophages, microglia, and astrocytes) and inflammatory mediators (matrix metalloproteinases, nuclear factor erythroid 2-related factor 2, heme oxygenase, and iron), and highlights the emerging areas of therapeutic promise.
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