Neurorestorative and protective effects of palmitoylethanolamide in perinatal asphyxia: An analysis of the rat striatum

Abstract

Perinatal asphyxia (PA) caused by low O2 availability during birth is associated with brain damage, been the striatum one of the most affected areas. Palmitoylethanolamide (PEA) is a neuroprotective amide in brain injury models, including PA. However, its effects against PA requires deeper study in the striatum. Using Bjelke? model, full-term pregnant rats were rapidly decapitated, and uterus horns placed in a water bath (37°C,19 min). One hour after, rats were treated with PEA (10 mg/kg,s.c.) and later given to surrogate mothers. 30d animals were perfused and coronal striatum sections as well as subcellular fractions were collected for immunohistochemistry and blotting (n=3). Phosphorylated high/medium molecular weight neurofilaments (pNF-H/M), Microtubule-Associated Protein 2 (MAP2), and Glial fibrillary acidic protein (GFAP) were analysed. All procedures were previously approved by our Institution. 2-way ANOVA followed by Tukey revealed a reduction in pNF-H/M and MAP2 reactive areas (45% and 70%), GFAP+ cells (20%) and reduced MAP2 and pNF-H/M immunocontents in PA-rat striatum. PEA totally restored GFAP+ cells and MAP2 immunoreaction and partially prevented the decreased pNF-H/M reactive area (78%) induced by PA. PEA also reversed the MAP2 reduction and partially prevented the decrease of pNF-H/M immunocontent induced by PA. No GFAP level alteration was detected. PEA treatment attenuated the striatum damage induced by PA, demonstrating its therapeutic potential against PA.