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

Journal of Inflammation

Research

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

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

DOI  :  10.1186/s12950-014-0035-2

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

来源: Springer

【 摘 要 】

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.

【 授权许可】

Unknown   
© Jing et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.