Cardioprotection mediated by ischemic post-conditioning and overexpression of trx-1 restore mitochondrial function in mice hearts.

GODOY E; PEREZ, V; VICO T; VANASCO V; ZAOBORNYJ T; CASANOVA V; CICALE E; GRECO MC; ALVAREZ S; GELPI RJ; D'ANNUNZIO V

buenos aires

Congreso; V International Congress in Translational Medicine; 2021

Internationa master of biomedical sciences (Freiburg university and Buenos Aires university)

Trx1 maintains the cellular redox state in homeostasis and its overexpression decreases the infarct size after an ischemia/reperfusion (I/R) injury. However, it reminds unclear if Trx1 is involved in ischemic postconditioning (PostC)-conferred cardioprotection in young and middle-age mice and which is its relationship with mitochondrial function.FVB (Wt) and transgenic mice that overexpress Trx1 and Trx1 mutated in their active site (DN-Trx1) were used, and were divided into young (4 months) and middle-age groups (12 months); n = 6 for each group. Using the Langendorff technique, hearts were subjected to 30 min of ischemia and 120 minutes of reperfusion (I/R group) or 30 min of ischemia with 6 cycles of R/I after I and 120min of reperfusion (PostC group). Infarct size was assessed using TTC. Mitochondrial function was measured polarographically with a Clark type electrode. Data is expressed as mean ± SEM and p