Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells

Ma, Yanmei; Ibeanu, Gordon C.; Wang, Liyao; Zhang, Jianzhong; Chang, Yun Woo; Dong, Jun; Li, P. Andy; Li, Jing

doi:10.1186/s12868-017-0337-4

Cited by 33 publications

(23 citation statements)

References 57 publications

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“…The results obtained herein also demonstrated an insignificant effect of Se treatment on hippocampal level of glutamate of treated CRS group, nevertheless, studies recorded that Se may indirectly counteracted glutamate induced neurotoxic insult in hippocampal neurons by different mechanism [80] , and that Se deficiency may increase the susceptibility to neurotoxic insults of glutamate [81] , these data may give the assumption that the effect of se on glutamate toxicity may be mediated indirectly through antagonizing its toxic effects rather than affecting its basal level.…”

supporting

confidence: 54%

The Prospective Protective Effect of Selenium Against Chronic Restraint Stress-Induced Memory Impairment in Male Albino Rats

Barhoma¹,

El-Esawy

2019

The Medical Journal of Cairo University

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Background: Selenium (Se) had underscored many beneficial neuroprotective potentials, particularly with respect to learning and memory. However, the protective effect of Se in memory impairment associated with Chronic Restraint Stress (CRS) is not yet elucidated. Aim of Study: The present study was carried out to examine the effect of Se treatment against CRS induced behavioral and biochemical abnormalities. Material and Methods: The stress was induced by restraining the animals in well ventilated tubes (6h/d) for consecutive 21 days. Animals were randomly divided into 4 groups (8 rats each): Normal control, drug control, CRS and Se treated CRS groups. After 21 days of the experiment, memory function was evaluated by Passive Avoidance (PA), T-maze and object recognition tasks. Hippocampal oxidative stress markers, Brain Derived Neurotrophic Factor (BDNF), amyloid P (AR) protein, phosphorylated TAU (p-TAU) protein as well as glutamate and acetylcholinestrase activity (AchE) levels were assessed. Results: This study revealed that the memory performance was markedly deteriorated in CRS group, accompanied by noticeable alterations in hippocampal oxidative stress markers, depleted levels of BDNF together with overproduction of A P , p-TAU and glutamate as well as, excessive activity of AchE enzyme. Meanwhile, these behavioral and biochemical deviations were alleviated under 21 days of Se co-treatment in CRS exposed rats. Conclusion: This study proved the beneficial protective effects of Se in CRS-induced memory deficits and its associated pathological changes in rats, which may draw the attention to Se as a new therapeutic candidate for memory dysfunction associated with stress and its related disorders.

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supporting

confidence: 54%

The Prospective Protective Effect of Selenium Against Chronic Restraint Stress-Induced Memory Impairment in Male Albino Rats

Barhoma¹,

El-Esawy

2019

The Medical Journal of Cairo University

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“…Mitochondria are increasingly recognized as key players in acquired kidney diseases (9). The structure of mitochondria is mainly regulated by cycles of fusion and fission (28). The role of mitochondrial fission in apoptosis has been confirmed by different laboratories in various apoptotic models (4).…”

Section: Discussionmentioning

confidence: 98%

p53/Drp1-dependent mitochondrial fission mediates aldosterone-induced podocyte injury and mitochondrial dysfunction

Yuan

Zhang

Jia

et al. 2018

American Journal of Physiology-Renal Physiology

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Mitochondrial dysfunction is increasingly recognized as an important factor in glomerular diseases. Previous study has shown that mitochondrial fission contributed to mitochondrial dysfunction. However, the mechanism of mitochondrial fission on mitochondrial dysfunction in aldosterone-induced podocyte injury remains ambiguous. This study aimed to investigate the pathogenic effect of mitochondrial fission both in vivo and in vitro. In an animal model of aldosterone-induced nephropathy, inhibition of the mitochondrial fission protein dynamin-related protein 1 (Drp1) suppressed aldosterone-induced podocyte injury. In cultured podocytes, aldosterone dose dependently induced Drp1 expression. Knockdown of Drp1 inhibited aldosterone-induced mitochondrial fission, mitochondrial dysfunction, and podocyte apoptosis. Furthermore, aldosterone dose dependently induced p53 expression. Knockdown of p53 inhibited aldosterone-induced Drp1 expression, mitochondrial dysfunction, and podocyte apoptosis. These findings implicated that aldosterone induced mitochondrial dysfunction and podocyte injury mediated by p53/Drp1-dependent mitochondrial fission, which may provide opportunities for therapeutic intervention for podocyte injury.

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“…Selenium was found to protect against neuronal hyperexcitability results from excessive production of glutamate. 83 In the same context, Ma et al 84 showed that selenium blocked neuronal loss and protected the hippocampal HT22 nerve cells against glutamate-induced mitochondrial dysfunction.…”

Section: Dovepressmentioning

confidence: 99%

<p>Selenium Nanoparticles Pre-Treatment Reverse Behavioral, Oxidative Damage, Neuronal Loss and Neurochemical Alterations in Pentylenetetrazole-Induced Epileptic Seizures in Mice</p>

Yuan¹,

Fu²,

Ji³

et al. 2020

IJN

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Introduction: Epilepsy is a chronic neurological condition characterized by behavioral, molecular, and neurochemical alterations. Current antiepileptic drugs are associated with various adverse impacts. The main goal of the current study is to investigate the possible anticonvulsant effect of selenium nanoparticles (SeNPs) against pentylenetetrazole (PTZ)mediated epileptic seizures in mice hippocampus. Sodium valproate (VPA) was used as a standard anti-epileptic drug. Methods: Mice were assigned into five groups (n=15): control, SeNPs (5 mg/kg, orally), PTZ (60 mg/kg, intraperitoneally), SeNPs+PTZ and VPA (200 mg/kg)+PTZ. All groups were treated for 10 days. Results: PTZ injection triggered a state of oxidative stress in the hippocampal tissue as represented by the elevated lipoperoxidation, heat shock protein 70 level, and nitric oxide formation while decreased glutathione level and antioxidant enzymes activity. Additionally, the blotting analysis showed downregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in the epileptic mice. A state of neuroinflammation was recorded following the developed seizures represented by the increased pro-inflammatory cytokines. Moreover, neuronal apoptosis was recorded following the development of epileptic convulsions. At the neurochemical level, acetylcholinesterase activity and monoamines content were decreased in the epileptic mice, accompanied by high glutamate and low GABA levels in the hippocampal tissue. However, SeNP supplementation was found to delay the onset and decreased the duration of tonic, myoclonic, and generalized seizures following PTZ injection. Moreover, SeNPs were found to provide neuroprotection through preventing the development of oxidative challenge via the upregulation of Nrf2 and HO-1, inhibiting the inflammatory response and apoptotic cascade. Additionally, SeNPs reversed the changes in the activity and levels of neuromodulators following the development of epileptic seizures. Conclusion: The obtained results suggest that SeNPs could be used as a promising anticonvulsant drug due to its potent antioxidant, anti-inflammatory, and neuromodulatory activities.

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Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells

Cited by 33 publications

References 57 publications

The Prospective Protective Effect of Selenium Against Chronic Restraint Stress-Induced Memory Impairment in Male Albino Rats

The Prospective Protective Effect of Selenium Against Chronic Restraint Stress-Induced Memory Impairment in Male Albino Rats

p53/Drp1-dependent mitochondrial fission mediates aldosterone-induced podocyte injury and mitochondrial dysfunction

<p>Selenium Nanoparticles Pre-Treatment Reverse Behavioral, Oxidative Damage, Neuronal Loss and Neurochemical Alterations in Pentylenetetrazole-Induced Epileptic Seizures in Mice</p>

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