Neuroprotective effect of Palmitoylethanolamide pretreatment on HT22 murine hippocampal cells subjected to hypoxia-reoxygenation

HERRERA MI AND UDOVIN LD (PRIMERA AUTORÍA COMPARTIDA); KOBIEC TAMARA; MARTÍNEZ MICAELA; CAMILA MENENDEZ-MAISSONAVE; TORO-URREGO, NICOLÁS; KUSNIER, CARLOS F.; KÖLLIKER-FRERS RODOLFO; OTERO-LOSADA, MATILDE; LUACES, JUAN PABLO; CAPANI FRANCISCO

Congreso; XXXVI Congreso Anual de la SAN (MODALIDAD VIRTUAL); 2021

Perinatal asphyxia (PA) is an oxygen deprivation that occurs around birth and altersneurodevelopment. Recent evidence from our laboratory revealed in vivo treatment withPalmitoylethanolamide (PEA) could attenuate early cytoskeletal dysfunction in CA1 hippocampalneurons and its behavioral correlate after PA (Herrera et al., 2018, 2020). In order to delve into theneuroprotective role of PEA against PA, we studied in vitro effects of PEA pretreatment in a murinehippocampal cell line HT22 subjected to hypoxia-reoxygenation. After incubation, cells underwenthypoxia for 24 h and 18 h of reoxygenation, or normoxia-reoxygenation in the respective controls.Cell viability was assessed using the MTT test. In a subsequent experiment, cultures were incubatedwith vehicle (absolute ethanol) or increasing doses of PEA (0.001, 0.1, 1, 10, 25, 50, 100 μM), 24 hbefore hypoxia-reoxygenation. Three cells were used for each dose tested and experiments wereperformed in triplicate. Our results revealed PEA pretreatment (100 μM) could significantly increasecell viability after hypoxia-reoxygenation. No toxic effect was observed in any of the tested doses.In a third experiment, cultures were incubated with vehicle (absolute ethanol) or PEA at a singleconcentration (100 μM) under the same experimental conditions. The number of viable cells wasquantified by the trypan blue method. Similar results were found, reinforcing the protective role ofPEA against hippocampal hypoxic insults.