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hemin/accident vasculaire cérébral
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Hemin toxicity: a preventable source of brain damage following hemorrhagic stroke.
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Hemorrhagic stroke is a common cause of permanent brain damage, with a significant amount of the damage occurring in the weeks following a stroke. This secondary damage is partly due to the toxic effects of hemin, a breakdown product of hemoglobin. The serum proteins hemopexin and albumin can bind
Neuroprotective effects of valproic acid against hemin toxicity: possible involvement of the down-regulation of heme oxygenase-1 by regulating ubiquitin-proteasomal pathway.
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During hemorrhagic stroke induced by intracerebral hemorrhage (ICH), brain injury occurs from the deleterious actions of hemoglobin byproducts; induction of heme oxygenase-1 (HO-1) also plays a critical role in the neurotoxicity in ICH. Valproic acid (VPA), which is a commonly used drug in the
The metabolism and toxicity of hemin in astrocytes.
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Hemin is cytotoxic, and contributes to the brain damage that accompanies hemorrhagic stroke. In order to better understand the basis of hemin toxicity in astrocytes, the present study quantified hemin metabolism and compared it to the pattern of cell death. Heme oxygenase-1 (HO-1) expression was
Phenanthrolines protect astrocytes from hemin without chelating iron.
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Hemin, the degradation product of hemoglobin, contributes to the neurodegeneration that occurs in the weeks following a hemorrhagic stroke. The breakdown of hemin in cells releases redox-active iron that can facilitate the production of toxic hydroxyl radicals. The present study used 3-week old
Cofilin signaling in hemin-induced microglial activation and inflammation.
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Intracerebral hemorrhage (ICH) is the most severe form of stroke and is further exacerbated by the secondary injury involving inflammatory response due to the activation of microglia. This secondary injury is partly due to the toxic effects of hemin, an endogenous breakdown product of hemoglobin.
Hemin inhibits the large conductance potassium channel in brain mitochondria: a putative novel mechanism of neurodegeneration.
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Intracerebral hemorrhage (ICH) is a pathological condition that accompanies certain neurological diseases like hemorrhagic stroke or brain trauma. Its effects are severely destructive to the brain and can be fatal. There is an entire spectrum of harmful factors which are associated with the
Coupling Between Interleukin-1R1 and Necrosome Complex Involves in Hemin-Induced Neuronal Necroptosis After Intracranial Hemorrhage.
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Background and Purpose- Accumulated evidence suggests that hemin-a breakdown product of hemoglobin-plays a pivotal role in the inflammatory injuries that result after hemorrhagic stroke through the Toll Like Receptor 2-Toll Like Receptor 4 signal pathway. However, the mechanism of how hemin triggers
Changes in mitochondrial ultrastructure in SH-SY5Y cells during apoptosis induced by hemin.
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Hemorrhagic stroke is associated with high morbidity and mortality. Hemin is a decomposition product of hemoglobin that is related to neuronal apoptosis after hemorrhage, although the molecular basis for this association remains unclear. To address this issue, the present study investigated
Hemopexin decreases hemin accumulation and catabolism by neural cells.
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Hemopexin is a serum, CSF, and neuronal protein that is protective after experimental stroke. Its efficacy in the latter has been linked to increased expression and activity of heme oxygenase (HO)-1, suggesting that it facilitates heme degradation and subsequent release of cytoprotective biliverdin
Uptake, metabolism and toxicity of hemin in cultured neurons.
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Following hemorrhagic stroke, red blood cells lyse and release neurotoxic hemin into the interstitial space. The present study investigates whether neurons can accumulate and metabolize hemin. We demonstrate that cultured neurons express the heme carrier protein 1 (HCP1), and that this transporter
Uptake and Toxicity of Hemin and Iron in Cultured Mouse Astrocytes.
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Hemin is a breakdown product of the blood protein, hemoglobin and is responsible for much of the secondary damage caused following a hemorrhagic stroke. Hemin is toxic to cultured astrocytes and it is thought that this toxicity is due to iron that is liberated when hemin is degraded. However, free
N-acetylcysteine targets 5 lipoxygenase-derived, toxic lipids and can synergize with prostaglandin E2 to inhibit ferroptosis and improve outcomes following hemorrhagic stroke in mice.
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OBJECTIVE
N-acetylcysteine (NAC) is a clinically approved thiol-containing redox modulatory compound currently in trials for many neurological and psychiatric disorders. Although generically labeled as an "antioxidant," poor understanding of its site(s) of action is a barrier to its use in
Deferasirox, a trivalent iron chelator, ameliorates neuronal damage in hemorrhagic stroke models
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Purpose: Intracranial hemorrhage (ICH) is a devastating disease with high mortality and morbidity. After ICH, iron released from the hematoma plays a crucial role in secondary brain injury. Deferasirox (DFR) is a trivalent iron chelator,
Neuronal Death After Hemorrhagic Stroke In Vitro and In Vivo Shares Features of Ferroptosis and Necroptosis.
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Intracerebral hemorrhage leads to disability or death with few established treatments. Adverse outcomes after intracerebral hemorrhage result from irreversible damage to neurons resulting from primary and secondary injury. Secondary injury has been attributed to hemoglobin and its oxidized product
Targeting heme oxygenase after intracerebral hemorrhage.
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Intracerebral hemorrhage (ICH) is the primary event in approximately 10% of strokes, and has higher rates of morbidity and mortality than ischemic stroke. Experimental evidence suggests that the toxicity of hemoglobin and its degradation products contributes to secondary injury that may be amenable
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