Abstract
BackgroundHyperglycemia exacerbates brain damage caused by cerebral ischemia. Neuroinflammation may play a role in mediating such enhanced damage. The objectives of this study were to examine the mRNA and protein levels and cell type distribution of ICAM-1 after cerebral ischemia in normo-and diabetic hyperglycemic rats.ResultsCompared to normoglycemic ischemia animals, diabetes aggravated neuronal death, decreased Nissl body staining, and increased ICAM-1 mRNA and protein levels in the frontal cortex. The increased ICAM-1 was located not only in vascular endothelial cells but also in cortical neurons.ConclusionsOur results suggest that exacerbated neuro-inflammation in the brain may mediate the detrimental effects of diabetes on the ischemic brain.
Highlights
Hyperglycemia exacerbates brain damage caused by cerebral ischemia
Transient forebrain ischemia for 8 min induced a mild brain edema at 1-day of reperfusion, which was identified by the increased swelling of the neuronal cell bodies and nucleus, and the widened intercellular space of the neurons, astrocytes and endothelial cells
The results showed that the intercellular cell adhesion molecule 1 (ICAM-1) mRNA levels were up-regulated after 1, 3, and 6 days of reperfusion in the normoglycemic rats and that diabetes further up-regulated the expression of the post-ischemic ICAM levels
Summary
Hyperglycemia exacerbates brain damage caused by cerebral ischemia. Studies have shown that hyperglycemia produces lactic acid, increases free radical formation, activates the intrinsic cell death pathway, disrupts the blood– brain barrier (BBB), and induces local inflammation [3]. Recent studies suggest that inflammation plays an important role in the occurrence and development of ischemic brain damage [2]. Cerebral ischemia results in vascular endothelial cell injury, leading to the expression of cell adhesion molecules and attracting PMN to attach to endothelial cells, which migrate to ischemic tissue where they: release pro-inflammatory cytokines, produce free radicals and activate microglia [5]. In addition to the activation of endothelial cells and trans-endothelial migration of PMN, the expression of ICAM-1 plays an important role in inducing neuro-inflammation and mediating the progression of ischemic injury after acute stroke [2]. Prevention of ICAM-1 expression by antisense infusion significantly decreases infarct size and the neurological deficits caused by transient focal ischemia [10,11]
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