1. Diabetes mitigates the recovery following intracranial hemorrhage in rats.
- Author
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Fan Z, Yuan Y, Wang F, Qi Y, Han H, Wu J, Zhang G, and Yang L
- Subjects
- Animals, Aquaporins metabolism, Blood-Brain Barrier pathology, Collagenases toxicity, Diabetes Mellitus, Experimental pathology, Disease Models, Animal, Gene Expression Regulation drug effects, In Situ Nick-End Labeling, Intracranial Hemorrhages chemically induced, Intracranial Hemorrhages pathology, Male, Occludin genetics, Occludin metabolism, Proliferating Cell Nuclear Antigen metabolism, Rats, Rats, Sprague-Dawley, Recovery of Function drug effects, Zonula Occludens-1 Protein genetics, Zonula Occludens-1 Protein metabolism, von Willebrand Factor metabolism, Diabetes Mellitus, Experimental physiopathology, Gene Expression Regulation physiology, Hippocampus metabolism, Intracranial Hemorrhages physiopathology, Recovery of Function physiology
- Abstract
Intracranial hemorrhage (ICH) is a common subtype of stroke with high morbidity and mortality. However, few studies have examined the effects of diabetes on the recovery from ICH-induced brain injury. Therefore, we examined the effects of diabetes on protein levels of aquaporins, neuronal loss, angiogenesis, blood brain barrier (BBB) integrity, and neurological deficits following intra-DH collagenase-induced ICH in the hippocampus. We found that diabetic rats exhibited enhanced AQP9 expression in the hippocampus relative to non-diabetic rats, which was associated with increased behavioral deficits. Additionally, ICH induced neovascularization, proliferation of brain microvascular endothelial cells, and hippocampal neuronal loss. However, ICH-induced neovascularization and proliferation of brain microvascular endothelial cells was severely impaired in diabetic rats. Furthermore, ICH-induced hippocampal neuronal loss was exaggerated in diabetic rats. Finally, ICH impaired BBB integrity in the ipsilateral hemisphere, which was increased in diabetic rats. Taken together, the attenuated brain angiogenesis, increased hippocampal neuronal loss, and impaired BBB integrity in diabetic rats after ICH were associated with enhanced AQP9 expression. This may suggest that AQP9 is one of the underlying mechanisms that can mitigate the recovery from ICH in diabetic populations., (Copyright © 2016. Published by Elsevier B.V.)
- Published
- 2017
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