THE ROLE OF THIOREDOXIN 1 IN THE ISCHEMIC POSTCONDITIONING ON DYSLIPIDEMIC MICE

MAZO TAMARA; PEREZ VIRGINIA; GOMEZ ANABELLA; MAGALI BARCHUK; GABRIELA BERG; D´ ANNUNZIO VERÓNICA; GELPI RICARDO J

Mar del Plata

Congreso; LXI REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA-V CONGRESO NACIONAL DE LA ASOCIACIÓN ARGENTINA DE CIENCIA Y TECNOLOGÍA DE ANIMALES DE LABORATORIO; 2016

SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA

It is known the damaged by reactive oxygen species duetoischemia/reperfusion (I/R) is exacerbating in dyslipidemia conditionand thereforeincreased infarct size. Regarding to cardioprotectionmechanism, it has beenshown that dyslipidemia could modifythe infarct size reduction conferred byIschemic postconditioning(IP). However, it has not been showed whether thelack of protectionif PI could be related with thioredoxin 1 system (Trx1).Thereforethe aim was to evaluate if IP exerts cardioprotective effectondyslipidemic mice and determine if these lack of reduction ofinfarct size arerelated to changes in Trx1 expression. C57 / BL6males mice were used, fed withcontrol diet or high-fat diet (HFD)during 12 weeks. We measured clinical biochemistry parametersand thehearts were subjected to 30 min of I and 120min R (Langendorff)(Group I/R, n=7), or an IP protocol (n=7, 6 Cycles of R/I,10 sec each). We assessed ventricular function, infarct size andTrx 1 expression (western blot, n = 5 per group). In HFD micedid total cholesterol, LDL and HDL increased compared to controlmice, but triglycerides did not change. The behavior of ventricularfunction was similar in all the groups. In control mice IP decreasedinfarct size compared to I/ R gorup (I/R: 55.2±2.6 vs.PI:40.2 ±1.6,p=0.05), however the cardioprotection was abolished in DAG mice(I/R: 67.0±4.0vs.PI:61.0±4.2) .In basal conditions, the Trx1 expressionwas higher in HFD mice compared with control group (control:0.79±0.14 vs.DAG: 1.98 ± 0.51p <0.05). In conclusion, our datasuggest that the cardioprotection afforded by PI is abolished inmice HFD, at least in part by inactivation of Trx1, since the antioxidantexpression did not change.