ArticleScientific reports2017
Anti-inflammatory and anti-excitoxic effects of diethyl oxopropanamide, an ethyl pyruvate bioisoster, exert robust neuroprotective effects in the postischemic brain.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Multitargeted Neuroprotective Strategies of Ethyl Pyruvate: From Molecular Mechanisms to Clinical Perspectives in CNS Disorders.Biomolecules & therapeutics · 2026Review
- Ethyl Pyruvate Attenuates Microglial NLRP3 Inflammasome Activation via Inhibition of HMGB1/NF-κB/miR-223 Signaling.Antioxidants (Basel, Switzerland) · 2021Article
- Ethyl pyruvate improves white matter remodeling in rats after traumatic brain injury.CNS neuroscience & therapeutics · 2021Article
- Ethyl Pyruvate Increases Post-Ischemic Levels of Mitochondrial Energy Metabolites: AMetabolites · 2020Article
- Sex-specific hippocampal metabolic signatures at the onset of systemic inflammation with lipopolysaccharide in the APPswe/PS1dE9 mouse model of Alzheimer's disease.Brain, behavior, and immunity · 2020Article
- Anti-Inflammatory and Neuroprotective Effects of DIPOPA (N,N-Diisopropyl-2-Oxopropanamide), an Ethyl Pyruvate Bioisoster, in the Postischemic Brain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Article
- Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway.Journal of physiology and biochemistry · 2018Article
- Ethyl pyruvate does not require microglia for mediating neuroprotection after excitotoxic injury.CNS neuroscience & therapeutics · 2017Article
- Extract of Spatholobus suberctus Dunn ameliorates ischemia-induced injury by targeting miR-494.PloS one · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ethyl pyruvate (EP) is a simple aliphatic ester of pyruvic acid and has been shown to have robust neuroprotective effects via its anti-inflammatory, anti-oxidative, and anti-apoptotic functions. In an effort to develop novel EP derivatives with greater protective potencies than EP, we generated four EP isosteres, among them the neuroprotective potency of N,N-diethyl-2-oxopropanamide (DEOPA), in which the ethoxy group of EP was replaced with diethylamine, was far greater than that of EP. When DEOPA was administered intravenously (5 mg/kg) to rat middle cerebral artery occlusion (MCAO) model at 6 hrs post-surgery, it suppressed infarct formation, ameliorated neurological and sensory/motor deficits, and inhibited microglial activation and neutrophil infiltrations in the postischemic brain more effectively than EP. In particular, DEOPA markedly suppressed LPS-induced nitrite production and cytokine/chemokine inductions in microglia, neutrophils, and endothelial cells and these effects are attributable to inhibition of the activity of NF-κB by suppressing IκB-α degradation and p65 to DNA binding. In addition, DEOPA suppressed NMDA-induced neuronal cell death in primary cortical neuron cultures by NAD replenishment and suppression of NF-κB activity. Together, these results indicate DEOPA has multi-modal protective effects against ischemic brain damage targeting numerous cell types in the brain and also against other inflammation-related diseases.
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