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

Journal of Inflammation

P Andy Li²  Feng-Ying Guo¹  Jian-Da Dong¹  Yue Chang¹  Cai-Xia Cao¹  Jian-Zhong Zhang¹  Jian-Gang Wang¹  Li Jing¹ 

[1] Department of Pathology, Ningxia Medical University and Ningxia Key Laboratory for Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia, P. R. China;Department of Pharmaceutical Sciences, Biomanufacturing Research Institute and Technological Enterprise (BRITE), North Carolina Central University, Durham, North Carolina, USA

关键词: Stroke;    Neuron;    Neurodegeneration;    Inflammation;    ICAM-1;    Forebrain ischemia;    Endothelia;    Cerebral ischemia;   

Others  :  1140718
DOI  :  10.1186/s12950-014-0035-2

 received in 2014-05-14, accepted in 2014-10-21,  发布年份 2014

【 摘 要 】

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.

【 授权许可】

   
2014 Jing et al.; licensee BioMed Central Ltd.

【 图 表 】

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