D-093 | Neuroprotective Effects of Palmitoylethanolamide on the Morphology and Viability of a Murine Hippocampal Neuronal Cell Line Subjected to Hypoxia

Disorders of the Nervous System
Author: Lucas Udovin | Email: lucas2304@hotmail.com

LUCAS UDOVIN^1°, JUAN PABLO LUACES^1°, TAMARA KOBIEC^1°3°,  SOFIA BORDET^1°3°, CLAUDIA MARDARAZ^1°, MALENA GARCIA^3°, FRANCISCO CAPANI^1°2°

^1° Centro de Altos Estudios en Ciencias Humanas y de la Salud, Universidad Abierta Interamericana, Consejo Nacional de Investigaciones Científicas y Técnicas, CAECIHS. UAI-CONICET, Buenos Aires, Argentina.
^2° Instituto de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, Santiago, Chile.
^3° Centro de Investigaciones en Psicología y Psicopedagogía (CIPP), Facultad de Psicología y Psicopedagogía, Pontificia Universidad Católica Argentina (UCA), Buenos Aires, Argentina

Perinatal asphyxia (PA) is an oxygen deprivation that occurs around birth and disrupts neurodevelopment. Recent evidence from our laboratory revealed that in vivo treatment with Palmitoylethanolamide (PEA) could attenuate early cytoskeletal dysfunction in CA1 hippocampal neurons and its behavioral correlate after PA (Herrera and Udovin et al. 2018, 2020, 2022). To further explore the neuroprotective role of PEA against PA, we studied the in vitro effects of PEA pretreatment in a murine hippocampal cell line HT22 subjected to hypoxia for 72 hours. The cultures were incubated with vehicle (absolute ethanol) or increasing doses of PEA (0.001, 0.1, 1, 10, 20 μM) for 72 hours before hypoxia and during the normoxia period. Cell viability was assessed using the trypan blue method. Our results revealed that PEA pretreatment (5, 10, and 20 μM) significantly attenuated the decrease in cell viability after hypoxia. Additionally, using immunofluorescence, the integrity of the actin cytoskeleton was evaluated using phalloidin toxin and the nuclear marker NeuN for nuclear integrity under the same experimental conditions mentioned above, and it was found that PEA at a single concentration (20 μM) was also able to attenuate the morphological alterations induced during hypoxia. Therefore, PEA appears to be a promising neuroprotective agent that requires further investigation of its mechanism for the implementation of future therapeutic strategies.