THE CARDIOPROTECTION CONFERRED BY THIOREDOXIN-1 IN ISCHEMIC POSTCONDITIONING IS ABOLISHED IN MIDDLE-AGED MICE.

ZAOBORNYJ T; CASANOVA V; D'ANNUNZIO V; MAZO T; GELPI RJ; PEREZ, V; GOMEZ A; CICALE E

Buenos Aires

Congreso; Reunion Conjunta de Sociedades de Biociencias; 2017

Thioredoxin-1 (Trx1) maintains the cellular redox status and decreasesthe 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. The aim was to study if Trx1is involved in the PostC cardioprotection mechanism and if the agecan modify this. Wild type mice hearts (Wt), transgenic mice heartsoverexpressing 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 weresubjected to 30 min of I and 120 of R (Langendorff technique) (I/Rgroup). In the PostC group, after I, a protocol of 6 cycles of R/I wasperformed. The assessment of the infarct size was performed usingTTC. Also, it was measure hidrogen peroxide (H2O2) production,protein nitration, Trx1 activity and expression and pAkt and pGSK3βexpression (western blot). Data are expressed as mean±SEM andp