Related Experiment Video For Cerebral ischemia
Updated: Apr 21, 2026
A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
Published on: July 14, 2016
Upregulation of ICAM-1 in diabetic rats after transient forebrain ischemia and reperfusion injury
Li Jing1, Jian-Gang Wang1, Jian-Zhong Zhang1
1Department of Pathology, Ningxia Medical University and Ningxia Key Laboratory for Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia P. R. China.
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.
