PMC:4277126 / 130057-130909 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4277126","sourcedb":"PMC","sourceid":"4277126","source_url":"http://www.ncbi.nlm.nih.gov/pmc/4277126","text":"Glutamate-induced neuronal injury\nGlutamate excitotoxicity is involved in many neurodegenerative diseases including AD. Attenuation of glutamate toxicity is one of the therapeutic strategies for AD. LBPs were administrated to detect if they can prevent neurotoxicity elicited by glutamate in primary cultured neurons.166 The glutamate-induced cell death as detected by LDH assay and caspase-3-like activity assay was significantly reduced by LBPs at concentrations ranging from 10 µg/mL to 500 µg/mL. LBPs provided neuroprotection even 1 hour after exposure to glutamate. In addition to glutamate, LBPs attenuated N-methyl-D-aspartate-induced neuronal damage, and glutamate-induced phosphorylation of JNK was reduced by treatment with LBPs (Figure 13). LBPs exerted significant neuroprotective effects on cultured cortical neurons exposed to 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