• Linyu Chen, Lina Wang, Xiangjian Zhang, Lili Cui, Yinxue Xing, Lipeng Dong, Zongjie Liu, Yanhua Li, Xiaolin Zhang, Chaohui Wang, Xue Bai, Jian Zhang, Lan Zhang, and Xumeng Zhao.
• Department of Neurology, Second Hospital of Hebei Medical University; Shijiazhuang, Hebei 050000, PR China.
• Brain Res. 2012 Sep 26;1475:80-7.

BackgroundInflammatory and oxidative damage play a pivotal role in cerebral ischemic pathogenesis and may represent a therapeutic target. Octreotide (OCT) has been proved to elicit a variety of biological effects through its anti-inflammatory and anti-oxidant properties in the treatment of severe acute pancreatitis and ischemia-reperfusion injury in retina and intestine. However little is known regarding the effect of OCT in ischemic stroke. Here, we designed this study to investigate the protective effect of OCT in ischemic stroke and explore the potential underlying mechanisms.MethodsMale Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (pMCAO) and randomly divided into four groups: Sham (sham-operated), MCAO (pMCAO+0.9% saline), OCT-L (pMCAO+OCT 50μg/kg) and OCT-H (pMCAO+OCT 100μg/kg) groups. OCT was administered intraperitoneally immediately after stroke. Neurological deficit scores, infarct volume and brain water content were measured at 24h after stroke. Immunohistochemical staining and western blot were used to analyze the expressions of Nrf2, HO-1 and NF-κB. SOD and MDA were measured by spectrophotometer.ResultsCompared with MCAO group, OCT significantly alleviated neurological deficit, lessened infarct volume and brain edema (P<0.05), upregulated the expression of Nrf2, HO-1 and SOD (P<0.05), and decreased the expression of NF-κB and MDA (P<0.05).ConclusionsOCT protected the brain against cerebral ischemic damage; this effect may be through upregulation of transcription factor Nrf2, HO-1 and downregulation of NF-κB expression.Copyright © 2012 Elsevier B.V. All rights reserved.

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