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 diab...

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Detalles Bibliográficos
Autores principales: Jing, Li, Wang, Jian-Gang, Zhang, Jian-Zhong, Cao, Cai-Xia, Chang, Yue, Dong, Jian-Da, Guo, Feng-Ying, Li, P Andy
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Research
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4226864/
https://www.ncbi.nlm.nih.gov/pubmed/25389378
http://dx.doi.org/10.1186/s12950-014-0035-2
Descripción
Sumario: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.

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