Journal
NEUROSCIENCE
Volume 250, Issue -, Pages 651-657Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2013.07.039
Keywords
hemorrhagic transformation; hyperglycemia; rosiglitazone; middle cerebral artery occlusion
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Funding
- National Natural Science Foundation of China [81171095]
- Zhejiang Provincial Natural Science Foundation of China [LR12H09001]
- Health Bureau of Zhejiang Province [WKJ2010-2-010, 2009A080]
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Hemorrhagic transformation (HT) has been claimed to represent the most feared complication of treatment with intravenous tissue plasminogen activator (t-PA) therapy. In this study, we tested the effect of rosiglitazone on HT in a rat focal cerebral ischemia model. Male Sprague Dawley rats received an injection of 50% dextrose (6 ml/kg intraperitoneally) and were subjected to middle cerebral artery occlusion (MCAO) 10 min later, with the regional cerebral blood flow monitored in vivo by laserDoppler-flowmetry. Two groups were included: rosiglitazone treatment and vehicle group. In the treatment group, after 1.5 h of ischemia, rosiglitazone (2 mg/kg) was administered at the onset of reperfusion. Neurobehavioral scores, infarct volume, hemoglobin leakage, hemorrhage rate, the expression of collagen IV and glucose transporter 1 (GLUT1) were measured at 24 h after ischemia. Rosiglitazone improved neurobehavioral deficits, reduced infarct volume and hemorrhage rate, and inhibited hemoglobin leakage, when compared with the vehicle group. In addition, it increased the expression of collagen IV and GLUT1 compared to the vehicle group. Our results suggest that rosiglitazone attenuated the hyperglycemia-induced HT after MCAO, possibly by preservation of GLUT1 expression. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
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