The effect of oleoylethanolamide administration in neuroinflammatory response after post-asphyctic brain injury.

EDUARDO BLANCO, INÉS HERRERA, JUAN IGNACIO ROMERO, LISANDRO GIRALDEZ, GESIVALDO SANTOS, PATRICIA RIVERA, JUAN SUÁREZ, PABLO GALEANO, FERNANDO RODRÍGUEZ DE FONSECA, FRANCISCO CAPANI

Mendoza

Conferencia; III Congreso Sociedad Argentina de Microscopia; 2014

SAMIC

Perinatal asphyxia (PA) is a leading cause of death and severe neurological impairments in children [1]. The incidence of severe PA is about 1/1000 live births, however an effective treatment has not yet been established [2,3]. The lipid transmitters modulate a wide range of physiological processes in mammals. In this sense, we have studied the involvement of acylethanolamide pathway in brain plasticity alterations induced by perinatal events. The aim of the current study was to evaluate the neuroprotective effects of oleoilethanolamide treatment (OEA 2 and 10 mg/kg) after perinatal asphyxia with rats. Pups were born by cesarean section (C+) or by cesarean section following 19 min of asphyxia (PA). Therefore, Iba1, a microglia specific marker, was assessed by immunohistochemistry in Prefrontal Cortex (ACC, anterior cingulate cortex) and dorsal Hippocampus (CA1). Results indicated that Iba1+ cells were reduced in ACC and CA1 regions of PA19 animals. OEA administration (2 mg/kg) induced an enhancement of Iba1+ cells in CA1 region of asphyctic animals, although it did not reach the level of control animals (C+ Veh and C+ OEA2) in ACC region (Fig. 1 and 2). It is concluded that the effects of low dose of OEA (OEA 2 mg/kg) could prevent neuroinflammation and facilitate neuronal repair in rats that had undergone acute birth asphyxia. Modulation of the acylethanolamide pathway could be a strategy against neonatal hypoxic-ischemic brain injury.