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Delayed administration of deferoxamine reduces brain damage and promotes functional recovery after transient focal cerebral ischemia in the rat.

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Title: Delayed administration of deferoxamine reduces brain damage and promotes functional recovery after transient focal cerebral ischemia in the rat.
Authors: Freret, Thomas (AUTHOR), Valable, Samuel (AUTHOR), Chazalviel, Laurent (AUTHOR), Saulnier, Romaric (AUTHOR), Mackenzie, Eric T. (AUTHOR), Petit, Edwige (AUTHOR), Bernaudin, Myriam (AUTHOR), Boulouard, Michel (AUTHOR), Schumann‐Bard, Pascale (AUTHOR)
Source: European Journal of Neuroscience. Apr2006, Vol. 23 Issue 7, p1757-1765. 9p. 1 Diagram, 1 Chart, 5 Graphs.
Subjects: Brain damage, Deferoxamine, Cerebral ischemia, Laboratory rats, Cerebral anoxia
Abstract: The mechanisms underlying functional recovery after stroke are poorly understood. Brain-adaptive responses to the hypoxic stress elicited by ischemia could contribute to these mechanisms. Indeed, hypoxia-inducible factor-1 (HIF-1), one of the main transcriptional factors regulated by oxygen level, increases the expression of several beneficial genes such as erythropoietin, glucose transporter-1 and vascular endothelial growth factor. In order to strengthen the expression of these hypoxia-inducible factors, we administered deferoxamine, an iron chelator known to stabilize HIF-1α protein expression, and examined its effects on the functional deficits induced by ischemia. Anesthetized Sprague–Dawley rats were subjected to 60 min of intraluminal occlusion of the middle cerebral artery. Chronic deferoxamine treatment (300 mg/kg, s.c.), or its vehicle, started 24 h after ischemia and was continued bi-weekly until the animals were killed. Sensorimotor deficits were periodically assessed over 2 months, and at this end point, the lesion volume was determined by histology. Treatment with deferoxamine significantly decreased the size of brain damage (−28%) after ischemia and improved behavioral recovery. Indeed, neurological score and sensorimotor performances in the adhesive removal test recovered earlier in the deferoxamine-treated animals. Moreover, the long-lasting skilled forepaw reaching deficits were attenuated by deferoxamine. Although an antioxidant effect of deferoxamine cannot be excluded, the hypothesis that its beneficial effects could be mediated by an increase in HIF-1 target genes merits further investigations. Our data suggest that delayed administration of deferoxamine could represent an interesting therapeutical approach to treat focal cerebral ischemia. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Delayed administration of deferoxamine reduces brain damage and promotes functional recovery after transient focal cerebral ischemia in the rat.
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  Data: <searchLink fieldCode="AR" term="%22Freret%2C+Thomas%22">Freret, Thomas</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Valable%2C+Samuel%22">Valable, Samuel</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Chazalviel%2C+Laurent%22">Chazalviel, Laurent</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Saulnier%2C+Romaric%22">Saulnier, Romaric</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Mackenzie%2C+Eric+T%2E%22">Mackenzie, Eric T.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Petit%2C+Edwige%22">Petit, Edwige</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Bernaudin%2C+Myriam%22">Bernaudin, Myriam</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Boulouard%2C+Michel%22">Boulouard, Michel</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Schumann‐Bard%2C+Pascale%22">Schumann‐Bard, Pascale</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Apr2006, Vol. 23 Issue 7, p1757-1765. 9p. 1 Diagram, 1 Chart, 5 Graphs.
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  Data: <searchLink fieldCode="DE" term="%22Brain+damage%22">Brain damage</searchLink><br /><searchLink fieldCode="DE" term="%22Deferoxamine%22">Deferoxamine</searchLink><br /><searchLink fieldCode="DE" term="%22Cerebral+ischemia%22">Cerebral ischemia</searchLink><br /><searchLink fieldCode="DE" term="%22Laboratory+rats%22">Laboratory rats</searchLink><br /><searchLink fieldCode="DE" term="%22Cerebral+anoxia%22">Cerebral anoxia</searchLink>
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  Data: The mechanisms underlying functional recovery after stroke are poorly understood. Brain-adaptive responses to the hypoxic stress elicited by ischemia could contribute to these mechanisms. Indeed, hypoxia-inducible factor-1 (HIF-1), one of the main transcriptional factors regulated by oxygen level, increases the expression of several beneficial genes such as erythropoietin, glucose transporter-1 and vascular endothelial growth factor. In order to strengthen the expression of these hypoxia-inducible factors, we administered deferoxamine, an iron chelator known to stabilize HIF-1α protein expression, and examined its effects on the functional deficits induced by ischemia. Anesthetized Sprague–Dawley rats were subjected to 60 min of intraluminal occlusion of the middle cerebral artery. Chronic deferoxamine treatment (300 mg/kg, s.c.), or its vehicle, started 24 h after ischemia and was continued bi-weekly until the animals were killed. Sensorimotor deficits were periodically assessed over 2 months, and at this end point, the lesion volume was determined by histology. Treatment with deferoxamine significantly decreased the size of brain damage (−28%) after ischemia and improved behavioral recovery. Indeed, neurological score and sensorimotor performances in the adhesive removal test recovered earlier in the deferoxamine-treated animals. Moreover, the long-lasting skilled forepaw reaching deficits were attenuated by deferoxamine. Although an antioxidant effect of deferoxamine cannot be excluded, the hypothesis that its beneficial effects could be mediated by an increase in HIF-1 target genes merits further investigations. Our data suggest that delayed administration of deferoxamine could represent an interesting therapeutical approach to treat focal cerebral ischemia. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1111/j.1460-9568.2006.04699.x
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        Text: English
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      – SubjectFull: Laboratory rats
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      – SubjectFull: Cerebral anoxia
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              Text: Apr2006
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