Is Selenium Supplementation Beneficial in Acute Ischemic Stroke?

Ramezani, Mahtab; Simani, Leila; Abedi, Sahar; Pakdaman, Hossein

doi:10.1097/nrl.0000000000000365

Cited by 8 publications

(8 citation statements)

References 39 publications

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“…In particular, total selenium intake above 300 μg/d and supplements and high doses of selenium are considered harmful and should be avoided. Evidence regarding the effect of selenium administration during the acute phase of stroke is limited, though promising results were demonstrated in two small RCTs [ 89 , 90 ].…”

Section: Discussionmentioning

confidence: 99%

“…Current literature provides limited evidence on the role of selenium supplementation during the acute phase of stroke. Two randomized placebo-controlled trials (RCTs) evaluated the effect of intravenous administration of sodium selenite pentahydrate (Selenase) on short-term and long-term acute ischemic stroke outcomes [ 89 , 90 ]. Both studies demonstrated that selenium supplementation improved short-term outcomes in acute stroke patients in the context of neurological deficits and degree of disability.…”

Section: The Role Of Selenium On Cerebrovascular Riskmentioning

confidence: 99%

“…Both studies demonstrated that selenium supplementation improved short-term outcomes in acute stroke patients in the context of neurological deficits and degree of disability. Additionally, Ramezani et al showed increased activity of antioxidant enzymes in patients who received Selenase, whereas serum inflammatory markers were lower in the Selenase group (N = 25) compared to the placebo group (N = 25) [ 90 ]. However, both studies failed to yield a beneficial effect of selenium supplementation during the acute phase of stroke in the context of long-term outcomes.…”

Section: The Role Of Selenium On Cerebrovascular Riskmentioning

confidence: 99%

See 2 more Smart Citations

Selenium, Stroke, and Infection: A Threefold Relationship; Where Do We Stand and Where Do We Go?

et al. 2023

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Stroke is currently the second most common cause of death worldwide and a major cause of serious long-term morbidity. Selenium is a trace element with pleotropic effects on human health. Selenium deficiency has been associated with a prothrombotic state and poor immune response, particularly during infection. Our aim was to synthesize current evidence on the tripartite interrelationship between selenium levels, stroke, and infection. Although evidence is contradictory, most studies support the association between lower serum selenium levels and stroke risk and outcomes. Conversely, limited evidence on the role of selenium supplementation in stroke indicates a potentially beneficial effect of selenium. Notably, the relationship between stroke risk and selenium levels is bimodal rather than linear, with higher levels of serum selenium linked to disturbances of glucose metabolism and high blood pressure, morbidities which are, in turn, substrates for stroke. Another such substrate is an infection, albeit forming a bidirectional relationship with both stroke and the consequences of impaired selenium metabolism. Perturbed selenium homeostasis leads to impaired immune fitness and antioxidant capacity, which both favor infection and inflammation; specific pathogens may also contend with the host for transcriptional control of the selenoproteome, adding a feed-forward loop to this described process. Broader consequences of infection such as endothelial dysfunction, hypercoagulation, and emergent cardiac dysfunction both provide stroke substrates and further feed-forward feedback to the consequences of deficient selenium metabolism. In this review, we provide a synthesis and interpretation of these outlined complex interrelationships that link selenium, stroke, and infection and attempt to decipher their potential impact on human health and disease. Selenium and the unique properties of its proteome could provide both biomarkers and treatment options in patients with stroke, infection, or both.

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Section: Discussionmentioning

confidence: 99%

Section: The Role Of Selenium On Cerebrovascular Riskmentioning

confidence: 99%

Section: The Role Of Selenium On Cerebrovascular Riskmentioning

confidence: 99%

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Selenium, Stroke, and Infection: A Threefold Relationship; Where Do We Stand and Where Do We Go?

et al. 2023

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“…Therefore, as an endogenous lipid-soluble antioxidant, CoQ 10 can effectively inhibit lipid peroxidation and is expected to be a drug that hinders ferroptosis ( Littarru and Tiano, 2007 ; Rizzardi et al, 2021 ). Another drug inhibiting ferroptosis during ischemic stroke is Se ( Ramezani et al, 2021 ). Alim et al found that Se supplementation activates GPX4 homeostatic transcription in vivo , inhibiting cellular ferroptosis and improving neurological function ( Alim et al, 2019 ).…”

Section: Treatment Of Ischemic Stroke By Targeting Ferroptosismentioning

confidence: 99%

New insights in ferroptosis: Potential therapeutic targets for the treatment of ischemic stroke

Wei

Xie²,

Wei³

et al. 2022

Front. Pharmacol.

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Stroke is a common disease in clinical practice, which seriously endangers people’s physical and mental health. The neurovascular unit (NVU) plays a key role in the occurrence and development of ischemic stroke. Different from other classical types of cell death such as apoptosis, necrosis, autophagy, and pyroptosis, ferroptosis is an iron-dependent lipid peroxidation-driven new form of cell death. Interestingly, the function of NVU and stroke development can be regulated by activating or inhibiting ferroptosis. This review systematically describes the NVU in ischemic stroke, provides a comprehensive overview of the regulatory mechanisms and key regulators of ferroptosis, and uncovers the role of ferroptosis in the NVU and the progression of ischemic stroke. We further discuss the latest progress in the intervention of ferroptosis as a therapeutic target for ischemic stroke and summarize the research progress and regulatory mechanism of ferroptosis inhibitors on stroke. In conclusion, ferroptosis, as a new form of cell death, plays a key role in ischemic stroke and is expected to become a new therapeutic target for this disease.

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“…Of these molecules, the ones with antioxidant activity particularly stand out. The anti-ischemic property of selenium, melatonin, natural and hemi-modified flavonoid antioxidants, and numerous synthetic agents has been demonstrated recently in different laboratory stroke-representing settings [ 5 , 6 , 7 , 8 ]. Hydroxypyridine derivatives have long been considered the molecules that act as membrane stabilizers to protect cellular and tissue integrity from inflammatory and hypoxic/ischemic damage [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Novel Hydroxypyridine Compound Protects Brain Cells against Ischemic Damage In Vitro and In Vivo

Blinova

Turovsky

Eliseikina

et al. 2022

IJMS

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A non-surgical pharmacological approach to control cellular vitality and functionality during ischemic and/or reperfusion-induced phases of strokes remains extremely important. The synthesis of 2-ethyl-6-methyl-3-hydroxypyridinium gammalactone-2,3-dehydro-L-gulonate (3-EA) was performed using a topochemical reaction. The cell-protective effects of 3-EA were studied on a model of glutamate excitotoxicity (GluTox) and glucose-oxygen deprivation (OGD) in a culture of NMRI mice cortical cells. Ca2+ dynamics was studied using fluorescent bioimaging and a Fura-2 probe, cell viability was assessed using cytochemical staining with propidium iodide, and gene expression was assessed by a real-time polymerase chain reaction. The compound anti-ischemic efficacy in vivo was evaluated on a model of irreversible middle cerebral artery (MCA) occlusion in Sprague-Dawley male rats. Brain morphological changes and antioxidant capacity were assessed one week after the pathology onset. The severity of neurological disorder was evaluated dynamically. 3-EA suppressed cortical cell death in a dose-dependent manner under the excitotoxic effect of glutamate and ischemia/reoxygenation. Pre-incubation of cerebral cortex cells with 10–100 µM 3-EA led to significant stagnation in Ca2+ concentration in a cytosol ([Ca2+]i) of neurons and astrocytes suffering GluTox and OGD. Decreasing intracellular Ca2+ and establishing a lower [Ca2+]i baseline inhibited necrotic cell death in an acute experiment. The mechanism of 3-EA cytoprotective action involved changes in the baseline and ischemia/reoxygenation-induced expression of genes encoding anti-apoptotic proteins and proteins of the oxidative status; this led to inhibition of the late irreversible stages of apoptosis. Incubation of brain cortex cells with 3-EA induced an overexpression of the anti-apoptotic genes BCL-2, STAT3, and SOCS3, whereas the expression of genes regulating necrosis and inflammation (TRAIL, MLKL, Cas-1, Cas-3, IL-1β and TNFa) were suppressed. 3-EA 18.0 mg/kg intravenous daily administration for 7 days following MCA occlusion preserved rats’ cortex neuron population, decreased the severity of neurological deficit, and spared antioxidant capacity of damaged tissues. 3-EA demonstrated proven short-term anti-ischemic activity in vivo and in vitro, which can be associated with antioxidant activity and the ability to target necrotic and apoptotic death. The compound may be considered a potential neuroprotective molecule for further pre-clinical investigation.

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Is Selenium Supplementation Beneficial in Acute Ischemic Stroke?

Cited by 8 publications

References 39 publications

Selenium, Stroke, and Infection: A Threefold Relationship; Where Do We Stand and Where Do We Go?

Selenium, Stroke, and Infection: A Threefold Relationship; Where Do We Stand and Where Do We Go?

New insights in ferroptosis: Potential therapeutic targets for the treatment of ischemic stroke

Novel Hydroxypyridine Compound Protects Brain Cells against Ischemic Damage In Vitro and In Vivo

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