Delayed postconditioning with cobalt chloride activates pro-survival pathways in a murine model of perinatal asphyxia

LOGICA, TAMARA; ROMERO, JUAN IGNACIO; HOLUBIEC, MARIANA; RIVIÈRE, STÉPHANIE; KOLLIKER FRES, RODOLFO; CASTILLA, ROCÍO; CAPANI, FRANCISCO

Mar del Plata, Buenos Aires

Congreso; XXX Congreso Sociedad Argentina de Investigación en Neurociencias (SAN); 2015

Sociedad Argentina de Investigación en Neurociencias

Perinatal asphyxia (PA) is an obstetric condition associated to a highmorbimortality rate (incidence of 1 to 5/1000 born alive) and is a significantrisk factor for various neurodevelopmental disorders. It has been noticed thata repetitive series of mild ischemic events applied after a mainhypoxic-ischemic event (post-conditioning) activates various neuroprotectivemechanisms, favoring neuronal survival and preserving memory and learningprocesses altered by PA. Cobalt chloride (CoCl2) might work as apost-conditioner since in normoxia it triggers transcriptional changesmimicking the organism response to a hypoxic event. For that reason we studiedthis compound as a possible neuroprotective therapy. To that end, SpragueDawley 7-day-old male rats were subjected to a hypoxia-ischemia (H-I) model byligation of the right common carotid artery and a subsequent acute asphyxia byexposure to a 100% N2 atmosphere for 3 minutes. 24 hours later60mg/kg of CoCl2 or vehicle were subcutaneously administered. After 1,4 and 24 hs, hippocampi were removed and the expression of HIF-1a, G3PDH Bcl2, Bax and P-AKT were analyzed bywestern blot. Postconditionated animals presented: an increase in Hif-1αexpression and G3PDH at 1 h and 24 h after the acute treatmentand a higher Bcl2/Bax ratio and P-AKT expression at 24 h post treatment. We canconclude that CoCl2 postconditioning activatespro-survival pathways in a murine model of PA.