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Autologous Blood Injection to Model Spontaneous Intracerebral Hemorrhage in Mice
Published on: August 24, 2011
Intracerebral hemorrhage in complement C3-deficient mice
1Department of Neurosurgery, University of Michigan Medical School, Ann Arbor, Michigan 48109-0532, USA.
Insights
Complement C3 deficiency reduces brain swelling and behavioral deficits after intracerebral hemorrhage (ICH) in mice. This suggests complement C3 plays a key role in ICH-induced brain injury.
Area of Science:
- Neuroscience
- Immunology
Background:
- Intracerebral hemorrhage (ICH) triggers the complement cascade, exacerbating brain damage.
- Complement C3 is a central component of this cascade and its role in ICH is investigated.
Purpose of the Study:
- To investigate the impact of complement C3 deficiency on brain damage following ICH.
- To assess brain edema, behavioral deficits, and molecular markers in C3-deficient mice post-ICH.
Main Methods:
- Male C3-deficient and C3-sufficient mice underwent autologous whole blood infusion into the basal ganglia to induce ICH.
- Brain water content and behavioral tests (forelimb use asymmetry, corner turn) were assessed.
- Heme oxygenase-1 (HO-1) expression was measured via Western blot and immunohistochemistry.
Main Results:
- C3-deficient mice exhibited significantly reduced brain water content in the ipsilateral basal ganglia 3 days post-ICH.
- Forelimb use asymmetry deficits were significantly lower in C3-deficient mice compared to controls.
- Heme oxygenase-1 (HO-1) levels were significantly decreased in C3-deficient mice.
Conclusions:
- Intracerebral hemorrhage induces less brain edema and behavioral impairments in complement C3-deficient mice.
- These findings highlight complement C3 as a critical mediator of brain injury following ICH.
Abstract:
The complement cascade is activated and contributes to brain damage after intracerebral hemorrhage (ICH). The present study investigated ICH-induced brain damage in complement C3-deficient mice. This study was divided into 2 parts. Male C3-deficient and C3-sufficient mice received an infusion of 30-microl autologous whole blood into the right basal ganglia. In the first part of our study, mice were killed 3 days later for brain water content measurement. Behavioral assessments including forelimb use asymmetry and corner turn tests were also preformed before and after ICH. In the second part of the study, brain heme oxygenase-1 (HO-1) was measured by Western blot analysis and immunohistochemistry 3 days after the infusion. We found that brain water content in the ipsilateral basal ganglia 3 days after ICH was less in C3-deficient mice compared to C3-sufficient mice (p < 0.05). The C3-deficient mice had reduced ICH-induced forelimb use asymmetry deficits compared with C3-sufficient mice (p < 0.05), although there was no significant difference in the corner turn test score. Western blot analysis showed that HO-1 contents were significantly lower in C3-deficient mice (day 3: 2024 +/- 560 vs. 5140 +/- 1151 pixels in the C3-sufficient mice, p < 0.05). We conclude that ICH causes less brain edema and behavioral deficits in complement C3-deficient mice. These results suggest that complement C3 is a key factor contributing to brain injury following ICH.
