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Updated: Jul 1, 2026
Modeling Intracerebral Hemorrhage in Mice: Injection of Autologous Blood or Bacterial Collagenase
Published on: September 22, 2012
Hyperglycemia in a NOD Mice Model of Type-I Diabetes Aggravates Collagenase-Induced Intracerebral Hemorrhagic Injury
Qasim M Alhadidi1,2, Kevin M Nash3, Ghaith A Bahader1
1Department of Medicinal and Biological Chemistry, College of Pharmacy and Pharmaceutical Sciences, University of Toledo, Toledo, OH 43606, USA.
Insights
Persistent hyperglycemia worsens outcomes after intracerebral hemorrhage (ICH) in a type 1 diabetes model. Diabetic mice experienced larger hematomas and poorer neurological function, indicating diabetes exacerbates ICH injury.
Area of Science:
- Neuroscience
- Endocrinology
- Pathology
Background:
- Intracerebral hemorrhage (ICH) is a severe stroke subtype with high mortality.
- Persistent hyperglycemia post-ICH correlates with worse neurological function and increased mortality.
- The molecular mechanisms by which hyperglycemia exacerbates ICH remain incompletely understood.
Purpose of the Study:
- To investigate the impact of type 1 diabetes mellitus on intracerebral hemorrhage (ICH) injury.
- To explore the molecular mechanisms underlying hyperglycemia-induced exacerbation of ICH.
Main Methods:
- Utilized a non-obese diabetic (NOD) mouse model of type 1 diabetes and non-diabetic controls.
- Induced ICH via intrastriatal collagenase injection.
- Assessed hematoma volume, neurobehavioral function (rotarod, grip strength), and glial cell activation (GFAP, Iba1) via immunohistochemistry.
Main Results:
- NOD mice exhibited significantly increased hematoma volume and impaired neurological function compared to controls.
- Reduced glial cell activation (GFAP, Iba1) was observed in diabetic mice.
- Expression of oxidative/nitrosative stress markers (3-nitrotyrosine, iNOS) was decreased in the diabetic group.
Conclusions:
- Hyperglycemia exacerbates ICH injury, leading to worsened neurological function.
- The molecular mechanisms of ICH injury in diabetic models differ from non-diabetic models, particularly regarding glial activation and oxidative stress.
Background:
Intracerebral hemorrhage (ICH) is a severe type of stroke with high mortality. Persistent hyperglycemia following ICH is linked to deteriorated neurological functions and death. However, the exacerbating effect of hyperglycemia on ICH injury at the molecular level is still unclear. Therefore, this study explores the impact of diabetes on ICH injury using a non-obese diabetic (NOD) mouse model of type I diabetes mellitus.
Methods:
NOD and non-diabetic (non-obese resistant) mice subjected to ICH by intrastriatal injection of collagenase were sacrificed three days following the ICH. Brains were collected for hematoma volume measurement and immunohistochemistry. Neurobehavioral assays were conducted 24 h before ICH and then repeated at 24, 48 and 72 h following ICH.
Results:
NOD mice showed increased hematoma volume and impairment in neurological function, as revealed by rotarod and grip strength analyses. Immunohistochemical staining showed reduced glial cell activation, as indicated by decreased GFAP and Iba1 staining. Furthermore, the expression of oxidative/nitrosative stress markers represented by 3-nitrotyrosine and inducible nitric oxide synthase was reduced in the diabetic group.
Conclusions:
Overall, our findings support the notion that hyperglycemia exacerbates ICH injury and worsens neurological function and that the mechanism of injury varies depending on the type of diabetes model used.
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