ArticleCNS neuroscience & therapeutics2017
Ethyl pyruvate does not require microglia for mediating neuroprotection after excitotoxic injury.
Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Ethyl pyruvate does not require microglia for mediating neuroprotection after excitotoxic injury.CNS neuroscience & therapeutics · 2017Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsEthyl pyruvate (EP) mediates protective effects after neuronal injury. Besides a direct conservation of damaged neurons, the modulation of indigenous glial cells has been suggested as one important mechanism for EP-related neuroprotection. However, the specific contribution of glial cells is still unknown.
methodsOrganotypic hippocampal slice cultures (OHSC) were excitotoxically lesioned by 50 μmol/L N-methyl-D-aspartate (NMDA, for 4 hours) or left untreated. In an additional OHSC subset, microglia was depleted using the bisphosphonate clodronate (100 μg/mL) before lesion. After removal of NMDA, EP containing culture medium (0.84 μmol/L, 8.4 μmol/L, 42 μmol/L, 84 μmol/L, 168 μmol/L) was added and incubated for 72 hours. OHSC were stained with propidium iodide to visualize degenerating neurons and isolectin IB
resultsEP significantly reduced neurodegeneration following induced excitotoxicity except for 168 μmol/L. For 84 μmol/L, a reduction in the microglia cells was observed. Microglia depletion did not affect neuronal survival after EP treatment. EP decelerated astrocytic wound closure at 48 hours after injury.
conclusionEP-mediated neuroprotection seems to be mediated by astrocytes and/or neurons.
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