Neuroprotective effects of palmitoylethanolamide in a murine hippocampal neuronal cell line subjected to hypoxia-reoxygenation

Perinatal asphyxia (PA), asphysia can be defined as a conditionof impaired gas exchange in a subject, which leads to progressivehypoxia, hypercapnia, and acidosis depending on the extent andduration of this interruption. Asphyxia may occur before, during or after delivery. Perinatal asphyxia is the most common cause of early neonatal death, but in survivors it can progress to hypoxicischaemic encephalopathy responsible for increased neurological morbidity. Palmitoylethanolamide (PEA) is an endogenous lipid compound that has shown neuroprotective properties inseveral models of encephalopathy in vivo and in vitro. In our laboratory, we found that administration within the first hour prevents long-term behavioural and morphological alterationsin rats subjected to perinatal asphyxia (PA), a neurological risk factor with increasing incidence worldwide and locally. In this project, we investigated the neuroprotective function of PEAby investigating cell viability and morphology in the murine hippocampal neuronal line HT22. Methodologically, different experimental groups were carried out, a control group treated with vehicle, and which was not subjected to hypoxia, a group that was subjected to hypoxia-reoxygenation and a group that was treated with PEA and subjected to hypoxia-reoxygenationand another control group that was treated with PEA and was not subjected to hypoxia. The results obtained in our experimental situation allowed us to conclude that PEA has a neuroprotectiveeffect on the murine hippocampal neuronal line HT22, as it partially attenuates the morphological alteration produced by hypoxia-reoxygenation. Therefore, PEA appears to be a promising neuroprotective agent requiring further investigation of its mechanism for the implementation of future strategies for its use.