Autophagy and ischemic preconditioning

D VELEZ; M BARREDA FRANK; S TARTAGLIA; HERMANN R; E. SAVINO; A VARELA; M.G MARINA PRENDES

Foz de Iguazu

Congreso; I Encuentro Panamericano de Ciencias Fisiológicas.; 2014

Ischemic preconditioning (IPC) is one of the interventionsmore powerful than reduces ischemia reperfusion injury.The aim of the present work was to study the involvement of autophagy (AF) in the cardioprotection exerted by the IPC and the preservation of mitochondrial morphology and ATP synthesis capacity.AF is considered a dynamic process that under physiological conditions is involved in the replacement of aged organelles or defective ones. Langendorff perfused hearts from female Wistar rats were used(250-300g body weight). The IPC consisted of 4 cycles of ischemia reperfusion of 5 min duration each, before ischemia sustained.Wortmannin (W), phosphatidylinositol 3-kinase (PI3K) inhibitor(100 nM), was used in the perfusion medium 5 min before PCI.The hearts were subjected to 25 min ofischemia and 60 min of reperfusion. The magnitude of the AF was assessedby the ratio of LC3II/LC3I and autophagic flux bythe disappearance of p62, at 30 and 60 min of reperfusion.Electronic microscopy were performed at the same time for assess mitochondrial damage. Statistical ANOVA was done (n = 6/group).Electronic microscopy showed greater conservation mitochondrial in the group undergoing PCI.The ratio LC3II/LC3I was higher in the PCI group, as well as the disappearance of p62 and the ATP synthesis.The results suggest that IPC could partly reduce injury by ischemia-reperfusion by decreasing mitochondrial damage and promoting AF.