subarachnoid hemorrhage/glutathione

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Vasospasm after subarachnoid hemorrhage in haptoglobin 2-2 mice can be prevented with a glutathione peroxidase mimetic.

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Vasospasm after subarachnoid hemorrhage (SAH) is attributable to inflammation and oxidative stress associated with extracellular hemoglobin (Hb). Haptoglobin (Hp) binds free Hb and the Hp-Hb complex is cleared by macrophages, and the Hp-2 isoform of Hp is associated with more oxidative stress and

Glutathione peroxidase and subarachnoid hemorrhage: implications for the role of oxidative stress in cerebral vasospasm.

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OBJECTIVE Worldwide, cerebral vasospasm after subarachnoid hemorrhage (SAH) has an estimated morbidity and mortality of 1.2 million annually. While it has long been suspected that reactive oxygen species play a major role in the etiology of cerebral vasospasm after SAH, promising results in animal

Neuroprotective role of glutathione peroxidase 4 in experimental subarachnoid hemorrhage models

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Background and purpose: Early brain injury is an essential pathological process after subarachnoid hemorrhage (SAH), with many cell death modalities. Ferroptosis is a newly discovered regulated cell death caused by the iron-dependent

Changes in glutathione peroxidase and lipid peroxides in cerebrospinal fluid and serum after subarachnoid hemorrhage--with special reference to the occurrence of cerebral vasospasm.

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SS31 attenuates oxidative stress and neuronal apoptosis in early brain injury following subarachnoid hemorrhage possibly by the mitochondrial pathway.

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SS31 has been shown to have neuroprotective effects in a number of neurological degenerative diseases. However, the mechanisms and its role of neuroprotection after subarachnoid hemorrhage (SAH) remain unexplored. The aim of the present study is to evaluate the neuroprotective effects

Astragaloside IV alleviates early brain injury following experimental subarachnoid hemorrhage in rats.

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Astragaloside IV, one of the main effective components isolated from Astragalus membranaceus, has multiple neuroprotective properties, while the effects of astragaloside IV on the attenuation of subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) and its possible mechanisms are unknown.

Reduction of intracellular glutathione levels produces sustained arterial narrowing.

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OBJECTIVE Although lipid peroxidation and alterations in endogenous antioxidants have been hypothesized to contribute to cerebral vasospasm after subarachnoid hemorrhage, there has been no direct evidence demonstrating the relationship between oxidative stress and delayed arterial narrowing. To

Malondialdehyde, glutathione peroxidase, and superoxide dismutase in cerebrospinal fluid during cerebral vasospasm in monkeys.

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Cerebral vasospasm may result from lipid peroxidation induced by oxyhemoglobin in the subarachnoid space after subarachnoid hemorrhage. To test this theory, vasospasm was induced in monkeys by intrathecal injections of oxyhemoglobin or supernatant fluid from autologous blood incubated in vitro.

Inhibition of BECN1 Suppresses Lipid Peroxidation by Increasing System Xc- Activity in Early Brain Injury after Subarachnoid Hemorrhage.

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Lipid peroxidation plays a crucial role in early brain injury (EBI) after subarachnoid hemorrhage (SAH), and cystine/glutamate antiporter system X_c^- has been proved to be associated with glutathione (GSH) synthesis, which protects cells against oxidative damage. Antioxidant

Effects of S-nitrosoglutathione on acute vasoconstriction and glutamate release after subarachnoid hemorrhage.

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OBJECTIVE Subarachnoid hemorrhage (SAH) causes acute vasoconstriction that contributes to ischemic brain injury shortly after the initial bleed. It has been theorized that decreased availability of nitric oxide (NO) may contribute to acute vasoconstriction. Therefore we examined the effect of the NO

Effect of Mannitol Infusion on Optic Nerve Injury After Acute Traumatic Subarachnoid Hemorrhage and Brain Injury.

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The primary aim of this paper is to investigate the neuroprotective and antiinflammatory effects of mannitol on optic nerve injury after acute traumatic subarachnoid hemorrhage and brain injury in rat models. Traumatic brain injury (TBI) and traumatic subarachnoid hemorrhage (tSAH) were produced by

Effects of 2-Aminoethyl Diphenylborinate, a Modulator of Transient Receptor Potential and Orai Channels in Subarachnoid Hemorrhage: An Experimental Study.

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BACKGROUND

Cerebral vasospasm remains a serious problem affecting morbidity and mortality in patients with subarachnoid hemorrhage (SAH) during neurosurgery. We aimed to demonstrate the role of the transient receptor potential channel and other channels for Ca²⁺ in the

The effects of Nigella sativa against oxidative injury in a rat model of subarachnoid hemorrhage.

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OBJECTIVE The aim of the study was to investigate the putative neuroprotective effect of Nigella sativa oil (NSO) treatment against subarachnoid hemorrhage (SAH) in rats. METHODS To induce SAH, rats were injected with 0.3 ml blood into their cisterna magna. Male Wistar albino rats were divided as

Cysteamine alleviates early brain injury via reducing oxidative stress and apoptosis in a rat experimental subarachnoid hemorrhage model.

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Oxidative stress plays an important role in the pathogenesis of early brain injury (EBI) following subarachnoid hemorrhage (SAH). The aim of this study was to assess whether cysteamine prevents post-SAH oxidative stress injury via its antioxidative and anti-apoptotic effects. It was observed that

Alpha lipoic acid alleviates oxidative stress and preserves blood brain permeability in rats with subarachnoid hemorrhage.

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The neuroprotective effect of alpha lipoic acid (ALA; 100 mg/kg, po), a dithiol antioxidant, on experimentally induced subarachnoid hemorrhage (SAH) was assessed in Wistar albino rats. Neurological examination scores recorded at the 48th h of SAH induction were increased in SAH groups, which were

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