Rutin and Selenium Co-administration Reverse 3-Nitropropionic Acid-Induced Neurochemical and Molecular Impairments in a Mouse Model of Huntington’s Disease

Abdelfattah, Mohamed S.; Badr, S.; Lotfy, S; Attia, Gouda H.; Aref, Ahmed; Moneim, Ahmed E. Abdel; Kassab, Rami B.

doi:10.1007/s12640-019-00086-y

Cited by 61 publications

(35 citation statements)

References 71 publications

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“…Asemi et al (2015), supplemented gestational diabetic patients with Se in a randomized control trial for six weeks and their results also showed an increase in GSH. This increase is correlated with the antioxidant effect of Se which allows Se to bind to ROS, thus preventing it from converting GSH to oxidizing GSH (GSSG) (Abdelfattah et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Hypoglycemic potential of selenium nanoparticles capped with polyvinyl-pyrrolidone in streptozotocin-induced experimental diabetes in rats

El-Borady

Othman

Atallah

et al. 2020

Heliyon

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This study was aimed to evaluate the efficacy of synthesized selenium nanoparticles (SeNPs) capped with glucose and polyvinyl-pyrrolidone (PVP) on the hyperglycemia and prooxidants/antioxidants imbalance present in model streptozotocin (STZ)-induced diabetic rats. SeNPs were synthesized and characterized. Twenty-four albino male rats were grouped into four different groups. After the rats were induced to have type 2 diabetes by STZ, the SeNPs-treated groups received a dose of 0.5 mg/ml of SeNPs for seven days. Plasma glucose and insulin levels, pancreatic insulin expression, the levels of lipid peroxidation (LPO), nitric oxide (NO), glutathione peroxidase (GPx) and glutathione (GSH) were evaluated. TEM images revealed the formation of semispherical particles with average size between 40 and 50 nm. SeNPs administration successfully reduced the hyperglycemia, raised the levels of insulin in both the pancreas and the plasma and restored the damaged pancreatic tissue. SeNPs also showed enhancement of the elimination of the diabetes-induced oxidative stress injuries by decreasing the pancreatic LPO and NO levels. Furthermore, the activities of the antioxidant enzyme GPx and GSH levels of the diabetic rats were increased. In conclusion, SeNPs capped with PVP could be used in the future as an agent that could manage Diabetes mellitus.

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Section: Discussionmentioning

confidence: 99%

Hypoglycemic potential of selenium nanoparticles capped with polyvinyl-pyrrolidone in streptozotocin-induced experimental diabetes in rats

El-Borady

Othman

Atallah

et al. 2020

Heliyon

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“…52 The antioxidant system including GSH, GPx, GR, SOD, and CAT protected against free radicals accumulation in the cell. 23 Depletion of GSH content and antioxidant enzymes activity in brain tissue is associated with epileptic seizures in human and animal models due to the excessive generation of ROS and this decrease was shown to increase with repetitive seizures. 24,53,54 On the other hand, SeNPs administration prior to PTZ was found to protect neuronal oxidative injury through inhibiting lipoperoxidation by-product (MDA), decreasing Hsp70 and NO formation accompanied by increasing GSH level.…”

Section: Dovepressmentioning

confidence: 99%

“…21 Moreover, SeNPs were found to enhance recovery of Alzheimer's disease through suppression of amyloid-β accumulation, in vitro. 22 Furthermore, therapeutic nanotechnology-based interventions can inhibit oxidative stress, neuroinflammation, and neuronal apoptosis may provide neuroprotection 23 and thus prevent the development of epileptic seizures. 24 Here, we aimed to investigate the potential neuroprotective and anticonvulsant activity of SeNPs against pentylenetetrazole (PTZ)-induced epileptic seizures through estimating the oxidative damage, neuroinflammation, neuronal apoptosis, cholinergic, as well as monoaminergic and amino acidergic transmission in the hippocampal tissue of mice.…”

Section: Introductionmentioning

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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“…It has been demonstrated that CPF is able to inhibit AChE activity by enhancing the phosphorylation of its serine site [26]. BDNF plays a key role in the survival of nerve cells and synaptic plasticity and has been involved in several neurological impairments such as Huntington, Alzheimer, and epilepsy [27]. CPF has been reported to inhibit the expression of BDNF in the cortical tissue of young rats [28].…”

mentioning

confidence: 99%

“…TNF-α is also a proinflammatory cytokine produced mainly from microglia and astrocytes. It regulates different physiological functions in the central nervous system including synaptic plasticity, memory, and learning [27]. Oversecretion of IL-1β and TNF-α is associated with several pathological conditions [54].…”

mentioning

confidence: 99%

Red Beetroot Extract Abrogates Chlorpyrifos-Induced Cortical Damage in Rats

Albasher

Al-Saleh

Alkubaisi

et al. 2020

Oxidative Medicine and Cellular Longevity

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Organophosphorus insecticides including chlorpyrifos (CPF) are mainly used for agriculture, household, and military purposes; their application is associated with various adverse reactions in animals and humans. This study was conducted to evaluate the potential neuroprotective effect of red beetroot methanolic extract (RBR) against CPF-induced cortical damage. Twenty-eight adult male Wistar albino rats were divided into 4 groups (n=7 in each group): the control group was administered physiological saline (0.9% NaCl), the CPF group was administered CPF (10 mg/kg), the RBR group was administered RBR (300 mg/kg), and the RBR+CPF group was treated with RBR (300 mg/kg) 1 hr before CPF (10 mg/kg) supplementation. All groups were treated for 28 days. Rats exposed to CPF exhibited a significant decrease in cortical acetylcholinesterase activity and brain-derived neurotrophic factor and a decrease in glial fibrillary acidic protein. CPF intoxication increased lipid peroxidation, inducible nitric oxide synthase expression, and nitric oxide production. This was accompanied by a decrease in glutathione content and in the activities of glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase in the cortical tissue. Additionally, CPF enhanced inflammatory response, indicated by increased levels and expression of interleukin-1β and tumor necrosis factor-α. CPF triggered neuronal apoptosis by upregulating Bax and caspase-3 and downregulating Bcl-2. However, RBR reversed the induced neuronal alterations following CPF intoxication. Our findings suggest that RBR can minimize and prevent CPF neurotoxicity through its antioxidant, anti-inflammatory, and antiapoptotic activities.

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Rutin and Selenium Co-administration Reverse 3-Nitropropionic Acid-Induced Neurochemical and Molecular Impairments in a Mouse Model of Huntington’s Disease

Cited by 61 publications

References 71 publications

Hypoglycemic potential of selenium nanoparticles capped with polyvinyl-pyrrolidone in streptozotocin-induced experimental diabetes in rats

Hypoglycemic potential of selenium nanoparticles capped with polyvinyl-pyrrolidone in streptozotocin-induced experimental diabetes in rats

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

Red Beetroot Extract Abrogates Chlorpyrifos-Induced Cortical Damage in Rats

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