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10.1186/s12974-016-0709-1 http://scihub22266oqcxt.onion/10.1186/s12974-016-0709-1 C5020472!5020472 !27618864     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27618864 &cmd=llinks): Failed to open stream: HTTP request failed! 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Heme oxygenase-1-mediated neuroprotection in subarachnoid hemorrhage via intracerebroventricular deferoxamine |pdf=|usr=}}{{27618864 }} gab.com Text Heme oxygenase-1-mediated neuroprotection in subarachnoid hemorrhage via intracerebroventricular deferoxamine JO: J Neuroinflammation http://www.kidney.de/pget.php?&tw=1&pmid=27618864 #FOAvip BACKGROUND: Subarachnoid hemorrhage (SAH) is a devastating disease that affects over 30,000 Americans per year. Previous animal studies have explored the therapeutic effects of deferoxamine (DFX) via its iron-chelating properties after SAH, but none have assessed the necessity of microglial/macrophage heme oxygenase-1 (HO-1 or Hmox1) in DFX neuroprotection, nor has the efficacy of an intracerebroventricular (ICV) administration route been fully examined. We explored the therapeutic efficacy of systemic and ICV DFX in a SAH mouse model and its effect on microglial/macrophage HO-1. METHODS: Wild-type (WT) mice were split into the following treatment groups: SAH sham?+?vehicle, SAH?+?vehicle, SAH?+?intraperitoneal (IP) DFX, and SAH?+?ICV DFX. For each experimental group, neuronal damage, cognitive outcome, vasospasm, cerebral and hematogenous myeloid cell populations, cerebral IL-6 concentration, and mitochondrial superoxide anion production were measured. HO-1 co-localization to microglia was measured using confocal images. Trans-wells with WT or HO-1(-/-) microglia and hippocampal neurons were treated with vehicle, red blood cells (RBCs), or RBCs with DFX; neuronal damage, TNF-? concentration, and microglial HO-1 expression were measured. HO-1 conditional knockouts were used to study myeloid, neuronal, and astrocyte HO-1 involvement in DFX-induced neuroprotection and cognitive recovery. RESULTS: DFX treatment after SAH decreased cortical damage and improved cognitive outcome after SAH yet had no effect on vasospasm; ICV DFX was most neuroprotective. ICV DFX treatment after SAH decreased cerebral IL-6 concentration and trended towards decreased mitochondrial superoxide anion production. ICV DFX treatment after SAH effected an increase in HO-1 co-localization to microglia. DFX treatment of WT microglia with RBCs in the trans-wells showed decreased neuronal damage; this effect was abolished in HO-1(-/-) microglia. ICV DFX after SAH decreased neuronal damage and improved cognition in Hmox1 (fl/fl) control and Nes (Cre) :Hmox1 (fl/fl) mice, but not LyzM (Cre) :Hmox1 (fl/fl) mice. CONCLUSIONS: DFX neuroprotection is independent of vasospasm. ICV DFX treatment provides superior neuroprotection in a mouse model of SAH. Mechanisms of DFX neuroprotection after SAH may involve microglial/macrophage HO-1 expression. Monitoring patient HO-1 expression during DFX treatment for hemorrhagic stroke may help clinicians identify patients that are more likely to respond to treatment. Twit Text FOAVip Heme oxygenase-1-mediated neuroprotection in subarachnoid hemorrhage via intracerebroventricular deferoxamine ????J Neuroinflammation http://www.kidney.de/pget.php?&tw=1&pmid=27618864 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27618864 #FOAvip English Wikipedia <ref>{{Cite pmid|27618864 }}</ref> Heme oxygenase-1-mediated neuroprotection in subarachnoid hemorrhage via intracerebroventricular deferoxamine #MMPMID27618864 LeBlanc RH 3rd ; Chen R ; Selim MH ; Hanafy KA J Neuroinflammation 2016[Sep]; 13 (1 ): 244 PMID27618864 show ga BACKGROUND: Subarachnoid hemorrhage (SAH) is a devastating disease that affects over 30,000 Americans per year. Previous animal studies have explored the therapeutic effects of deferoxamine (DFX) via its iron-chelating properties after SAH, but none have assessed the necessity of microglial/macrophage heme oxygenase-1 (HO-1 or Hmox1) in DFX neuroprotection, nor has the efficacy of an intracerebroventricular (ICV) administration route been fully examined. We explored the therapeutic efficacy of systemic and ICV DFX in a SAH mouse model and its effect on microglial/macrophage HO-1. METHODS: Wild-type (WT) mice were split into the following treatment groups: SAH sham?+?vehicle, SAH?+?vehicle, SAH?+?intraperitoneal (IP) DFX, and SAH?+?ICV DFX. For each experimental group, neuronal damage, cognitive outcome, vasospasm, cerebral and hematogenous myeloid cell populations, cerebral IL-6 concentration, and mitochondrial superoxide anion production were measured. HO-1 co-localization to microglia was measured using confocal images. Trans-wells with WT or HO-1(-/-) microglia and hippocampal neurons were treated with vehicle, red blood cells (RBCs), or RBCs with DFX; neuronal damage, TNF-? concentration, and microglial HO-1 expression were measured. HO-1 conditional knockouts were used to study myeloid, neuronal, and astrocyte HO-1 involvement in DFX-induced neuroprotection and cognitive recovery. RESULTS: DFX treatment after SAH decreased cortical damage and improved cognitive outcome after SAH yet had no effect on vasospasm; ICV DFX was most neuroprotective. ICV DFX treatment after SAH decreased cerebral IL-6 concentration and trended towards decreased mitochondrial superoxide anion production. ICV DFX treatment after SAH effected an increase in HO-1 co-localization to microglia. DFX treatment of WT microglia with RBCs in the trans-wells showed decreased neuronal damage; this effect was abolished in HO-1(-/-) microglia. ICV DFX after SAH decreased neuronal damage and improved cognition in Hmox1 (fl/fl) control and Nes (Cre) :Hmox1 (fl/fl) mice, but not LyzM (Cre) :Hmox1 (fl/fl) mice. CONCLUSIONS: DFX neuroprotection is independent of vasospasm. ICV DFX treatment provides superior neuroprotection in a mouse model of SAH. Mechanisms of DFX neuroprotection after SAH may involve microglial/macrophage HO-1 expression. Monitoring patient HO-1 expression during DFX treatment for hemorrhagic stroke may help clinicians identify patients that are more likely to respond to treatment. |Animals [MESH] |Calcium-Binding Proteins/metabolism [MESH] |Cells, Cultured [MESH] |Cognition Disorders/etiology/prevention & control [MESH] |Deferoxamine/*administration & dosage [MESH] |Disease Models, Animal [MESH] |Dose-Response Relationship, Drug [MESH] |Heme Oxygenase-1/genetics/*metabolism [MESH] |Injections, Intraventricular [MESH] |Male [MESH] |Maze Learning/drug effects [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Microfilament Proteins/metabolism [MESH] |Microglia/drug effects [MESH] |Neuroprotective Agents/*administration & dosage [MESH]Heme oxygenase-1-mediated neuroprotection in subarachnoid hemorrhage v(epmc).pdf DeepDyve Pubget Overpricing