The protection by Octreotide against experimental ischemic stroke: Up-regulated transcription factor Nrf2, HO-1 and down-regulated NF-κB expression

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. Methods: Male 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 50 μg/kg) and OCT-H (pMCAO+OCT 100 μg/kg) groups. OCT was administered intraperitoneally immediately after stroke. Neurological deficit scores, infarct volume and brain water content were measured at 24 h 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. Results: Compared 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). Conclusions: OCT 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.

► Rat pMCAO model is used to analyse octreotide’s protective effect.
► Octreotide ameliorates the neurological deficit, brain edema and infarct volume.
► Octreotide upregulates Nrf2, HO-1, SOD and downregulates MDA expression.
► Octreotide downregulates NF-κB expression.
► Octreotide has protective effect in the acute phase of cerebral ischemia.