Upregulation of ICAM-1 in diabetic rats after transient forebrain ischemia and reperfusion injury.
BACKGROUND
Hyperglycemia 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.


RESULTS
Compared 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.


CONCLUSIONS
Our results suggest that exacerbated neuro-inflammation in the brain may mediate the detrimental effects of diabetes on the ischemic brain.
['Jing|Li|L|', 'Wang|Jian-Gang|JG|', 'Zhang|Jian-Zhong|JZ|', 'Cao|Cai-Xia|CX|', 'Chang|Yue|Y|', 'Dong|Jian-Da|JD|', 'Guo|Feng-Ying|FY|', 'Li|P Andy|PA|']
ICAM-1 Forebrain ischemia Cerebral ischemia Neuron Endothelia Inflammation Neurodegeneration Stroke