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. 2019 Feb 7;13:64. doi: 10.3389/fnins.2019.00064

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Copyright © 2019 Khansari and Halliwell.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Impact of Cyclooxygenase inhibition on glutamate-evoked neurotoxicity: hippocampal neurons 9 days in culture were exposed to glutamate (5 μM) in the absence (control) or presence of either sodium salicylate (SAL), indomethacin (INDO), or ibuprofen (IBU) (each at 10 and 100 μM). Drugs were co-incubated during glutamate exposure and immediately after exposure for 24 h. Cell death was measured 24 h post-exposure using Cytotox-96. Sodium salicylate significantly reduced cell death by 56% (^∗∗p ≤ 0.01) and 65% (^∗∗p ≤ 0.01) at 10 and 100 μM, respectively. However, neither indomethacin nor ibuprofen reduced glutamate-induced cell death. The NMDA channel blocker, MK-801 (10 μM) reduced cell death by 98% (^∗∗p ≤ 0.01).