ArticleNeurotoxicity research2017
N-Adamantyl-4-Methylthiazol-2-Amine Attenuates Glutamate-Induced Oxidative Stress and Inflammation in the Brain.
Article in Neurotoxicity research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Therapeutic effects ofIBRO neuroscience reports · 2025Article
- Electrochemical detection of the neurotransmitter glutamate and the effect of the psychotropic drug riluzole on its oxidation response.Analytical and bioanalytical chemistry · 2024Article
- Glutamate Efflux across the Blood-Brain Barrier: New Perspectives on the Relationship between Depression and the Glutamatergic System.Metabolites · 2022Review
- Is L-Glutamate Toxic to Neurons and Thereby Contributes to Neuronal Loss and Neurodegeneration? A Systematic Review.Brain sciences · 2022Review
- N-Adamantyl-4-methylthiazol-2-amine suppresses glutamate-induced autophagic cell death via PI3K/Akt/mTOR signaling pathways in cortical neurons.BMB reports · 2020Article
- TRPV1 Contributes to Cerebral Malaria Severity and Mortality by Regulating Brain Inflammation.Oxidative medicine and cellular longevity · 2019Article
- Homeostasis of the Intraparenchymal-Blood Glutamate Concentration Gradient: Maintenance, Imbalance, and Regulation.Frontiers in molecular neuroscience · 2017Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we explored the possible mechanisms underlying the neuroprotective and anti-oxidative effects of N-adamantyl-4-methylthiazol-2-amine (KHG26693) against in vivo glutamate-induced toxicity in the rat cerebral cortex. Our results showed that pretreatment with KHG26693 significantly attenuated glutamate-induced elevation of lipid peroxidation, tumor necrosis factor-α, interferon gamma, IFN-γ, interleukin-1β, nitric oxide, reactive oxygen species, NADPH oxidase, caspase-3, calpain activity, and Bax. Furthermore, KHG26693 pretreatment attenuated key antioxidant parameters such as levels of superoxide dismutase, catalase, glutathione, and glutathione reductase. KHG26693 also attenuated the protein levels of inducible nitric oxide synthase, neuronal nitric oxide synthase, nuclear factor erythroid 2-related factor 2, heme oxygenase-1, and glutamate cysteine ligase catalytic subunit caused by glutamate toxicity. Finally, KHG26693 mitigated glutamate-induced changes in mitochondrial ATP level and cytochrome oxidase c. Thus, KHG26693 functions as neuroprotective and anti-oxidative agent against glutamate-induced toxicity through its antioxidant and anti-inflammatory activities in rat brain at least in part.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.