ArticleMetabolic brain disease2017
Selenium attenuates apoptosis, inflammation and oxidative stress in the blood and brain of aged rats with scopolamine-induced dementia.
Article in Metabolic brain disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 75 citations in OpenAlex.
- Study on the molecular aspect of cardioprotective effects of selenium: a mini-review.Journal of basic and clinical physiology and pharmacology · 2025Review
- Acceleration-Dependent Effects of Vibrotactile Gamma Stimulation on Cognitive Recovery and Cholinergic Function in a Scopolamine-Induced Neurotoxicity Mouse Model.Biomedicines · 2025Article
- Neuroprotective Potential of Phytocompounds in the Treatment of Dementia: The State of Knowledge from the Scopolamine-Induced Animal Model of Alzheimer's Disease.Current issues in molecular biology · 2025Review
- Pioglitazone improves learning and memory in a rat model of cholinergic dysfunction induced by scopolamine, the roles of oxidative stress and neuroinflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Selenium Nanoparticles as Neuroprotective Agents: Insights into Molecular Mechanisms for Parkinson's Disease Treatment.Molecular neurobiology · 2025Review
- Anethole Ameliorates Scopolamine-Induced Memory Deficits and Neuronal Damage Through Antioxidant, Anti-Inflammatory, and Anticholinesterase Activities in Rats.Neurochemical research · 2025Article
- Selenium reduces oxaliplatin induced neuropathic pain: focus on TRPV1.Frontiers in pharmacology · 2025Article
- Epigallocatechin-3-gallate conjugated with selenium nanoparticles prevents neurological complications in rats exhibiting schizophrenia-like behaviors.Frontiers in pharmacology · 2025Article
- Resveratrol-Loaded Pluronic Micelles Ameliorate Scopolamine-Induced Cognitive Dysfunction Targeting Acetylcholinesterase Activity and Programmed Cell Death.International journal of molecular sciences · 2024Article
- Comparison of Malondialdehyde, Acetylcholinesterase, and Apoptosis-Related Markers in the Cortex and Hippocampus of Cognitively Dysfunctional Mice Induced by Scopolamine.Biomedicines · 2024Article
- Ameliorating Effect of Sodium Selenite on Developmental and Molecular Response of Bovine Cumulus-Oocyte Complexes Matured in Vitro Under Heat Stress Condition.Biological trace element research · 2024Article
- Neuroprotective Effects ofPharmaceuticals (Basel, Switzerland) · 2023Article
- Dietary Protection against Cognitive Impairment, Neuroinflammation and Oxidative Stress in Alzheimer's Disease Animal Models of Lipopolysaccharide-Induced Inflammation.International journal of molecular sciences · 2023Review
- Effect of Sinapic Acid on Scopolamine-Induced Learning and Memory Impairment in SD Rats.Brain sciences · 2023Article
- Effects ofCurrent issues in molecular biology · 2023Article
- Effects of long-termSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- Neuroprotective effect of ranolazine improves behavioral discrepancies in a rat model of scopolamine-induced dementia.Frontiers in neuroscience · 2023Article
- An aqueous macerate of Ziziphus jujuba reduces long-term spatial memory impairment in D-galactose treated rats: role of anti-inflammatory pathways.Metabolic brain disease · 2022Article
- The Potential Neuroprotective Effect ofMolecules (Basel, Switzerland) · 2022Article
- Rosiridin Attenuates Scopolamine-Induced Cognitive Impairments in Rats via Inhibition of Oxidative and Nitrative Stress Leaded Caspase-3/9 and TNF-α Signaling Pathways.Molecules (Basel, Switzerland) · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A potent antioxidant, selenium might modulate dementia-induced progression of brain and blood oxidative and apoptotic injuries. The present study explores whether selenium protects against experimental dementia (scopolamine, SCOP)-induced brain, and blood oxidative stress, apoptosis levels, and cytokine production in rats. Thirty-two rats were equally divided into four groups. The first group was used as an untreated control. The second group was treated with SCOP to induce dementia. The third and fourth groups received 1.5 mg/kg selenium (sodium selenite) and SCOP + selenium, respectively. Dementia was induced in the second and forth groups by intraperitoneal SCOP (1 mg/kg) administration. Brain, plasma, and erythrocyte lipid peroxidation levels as well as plasma TNF-α, interleukin (IL)-1β, and IL-4 levels were high in the SCOP group though they were low in selenium treatments. Selenium and selenium + SCOP treatments increased the lowered glutathione peroxidase activity, reduced glutathione, vitamins A and E concentrations in the brain, erythrocytes and plasma of the SCOP group. Apoptotic value expressions as active caspase-3, procaspase-9, and PARP were also increased by SCOP, while they were decreased by selenium and selenium + SCOP treatments. In conclusion, selenium induced protective effects against experimental dementia-induced brain, and blood oxidative injuries and apoptosis through regulation of cytokine production, vitamin E, glutathione concentrations, and glutathione peroxidase activity.
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