Thioredoxin-1 is involved in cardioprotection conferred by ischemic postconditioning.

PEREZ, VIRGINIA; D'ANNUNZIO, VERONICA; MAZO, TAMARA; MARCHINI, TIMOTEO; CACERES, LOURDES; EVELSON, PABLO; GELPI, RICARDO

Mar del Plata

Congreso; LXI Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica; 2016

Sociedad Argentina de Investigación Clinica

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). The aim was to study if Trx1 is involved in the PostC cardioprotection mechanism. Wild type mice hearts (Wt), transgenic mice hearts overexpressing Trx1, and a dominant negative (DN-Trx1) mutant (C32S/C35S) of Trx1 were used. The mice hearts were subjected to 30 min of I and 120 of R (Langendorff technique) (I/R group). In the PostC group, after I, a protocol of 6 cycles of R/I (15 sec and 10 sec each), was performed. The assessment of the infarct size was performed using TTC. Reduced (GSH) and oxidized (GSSG) glutathione levels were measured by HPLC and Trx, pAkt and pGSK3beta expression were evaluated by western blot. Data are expressed as mean ± SEM and p