Department of Neurology, The Second Affiliated Hospital, Zhejiang University, School of Medicine, Hangzhou 310009, People's Republic of China; Department of Neurology, The Affiliated Children's Hospital, Zhejiang University, School of Medicine, Hangzhou 310003, People's Republic of China.
Neuroscience. 2013 Oct 10;250:651-7. doi: 10.1016/j.neuroscience.2013.07.039. Epub 2013 Jul 25.
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 (6ml/kg intraperitoneally) and were subjected to middle cerebral artery occlusion (MCAO) 10 min later, with the regional cerebral blood flow monitored in vivo by laser-Doppler-flowmetry. Two groups were included: rosiglitazone treatment and vehicle group. In the treatment group, after 1.5h of ischemia, rosiglitazone (2mg/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 24h 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.
出血性转化（HT）被认为是静脉注射组织型纤溶酶原激活剂（t-PA）治疗最可怕的并发症。在这项研究中，我们在大鼠局灶性脑缺血模型中测试了罗格列酮对 HT 的影响。雄性 Sprague-Dawley 大鼠接受 50%葡萄糖（6ml/kg 腹腔内注射），10 分钟后进行大脑中动脉闭塞（MCAO），通过激光多普勒血流仪在体内监测局部脑血流。包括两组：罗格列酮治疗组和载体组。在治疗组中，缺血 1.5 小时后，再灌注开始时给予罗格列酮（2mg/kg）。在缺血后 24 小时测量神经行为评分、梗死体积、血红蛋白渗漏、出血率、胶原 IV 和葡萄糖转运蛋白 1（GLUT1）的表达。与载体组相比，罗格列酮改善了神经行为缺陷，减少了梗死体积和出血率，并抑制了血红蛋白渗漏。此外，与载体组相比，它增加了胶原 IV 和 GLUT1 的表达。我们的结果表明，罗格列酮减轻了 MCAO 后高血糖引起的 HT，可能是通过保存 GLUT1 的表达。
