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CNS neuroscience & therapeutics

Ethyl pyruvate does not require microglia for mediating neuroprotection after excitotoxic injury.


PMID 28836378

Abstract

Ethyl 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. Organotypic 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 EP 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. EP-mediated neuroprotection seems to be mediated by astrocytes and/or neurons.

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