The cardioprotection mediated by ischemic postconditioning and Trx1 overexpression restore mitochondrial function in mice heart

GOMEZ A; VANASCO V; CASANOVA V; ALVAREZ S; MAZO T; ZAOBORNYJ T; CICALE E; D´ANNUNZIO V; PEREZ MV; VICO T; AYELEN C; GRECCO C; GELPI RJ

Congreso; LXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2019

Sociedad Argentina de Investigación Clínica (SAIC)

Thioredoxin-1 (Trx1) maintains the cellular redox status and decreases the infarct size in ischemia/reperfusion injury (I/R). However, it is not fully understood the role of Trx1 in ischemic postconditioning (PostC) in young and aged mice and its relation with mitochondrial function. The aim was to study if Trx1 is involved in the PostC cardioprotection mechanism and can restore mitochondrial function and if the age can modify this. Wild type mice hearts (Wt), transgenic mice hearts overexpressing Trx1, and a dominant negative (DN-Trx1) mutant (C32S/C35S) of Trx1 were used, mice were divided in young group (4 month) and middle-aged group (12 month). The mice hearts were subjected to 30min of I and 120min of R (Langendorff technique) (I/R group). In the PostC group, after I, a protocol of 6 cycles of R/I was performed. The assessment of the infarct size was performed using TTC. Also, it was mitochondrial function (pollarographically with a Clark-type electrode). Data are expressed as mean±SEM and p