It has been demonstrated that a short-timed ischemia, also called preconditioning (PC), may exert a protective role against a subsequent prolonged stress. This phenomenon is the strongest form of in vivo protection against myocardial ischemic injury. The ischemic PC concept has been extended to PC triggered by non-ischemic stress, such as stretch, some chemicals, hypoxia, and reactive oxygen radicals. The present study was designed to investigate the mechanisms behind hydrogen peroxide preconditioning cardioprotection focusing on antioxidant and phase II enzyme induction and their modulation by mitogen activated protein kinases (MAPKs) and phosphatidylinositol 3-kinase (PI3K)/Akt.
H2O2 preconditioning protects cardiomyocytes through phase II enzyme induction and p38 MAPK and Akt signalling.
FABBRI, DANIELE;ANGELONI, CRISTINA;MOTORI, ELISA;MALAGUTI, MARCO;LEONCINI, EMANUELA;HRELIA, SILVANA
2010
Abstract
It has been demonstrated that a short-timed ischemia, also called preconditioning (PC), may exert a protective role against a subsequent prolonged stress. This phenomenon is the strongest form of in vivo protection against myocardial ischemic injury. The ischemic PC concept has been extended to PC triggered by non-ischemic stress, such as stretch, some chemicals, hypoxia, and reactive oxygen radicals. The present study was designed to investigate the mechanisms behind hydrogen peroxide preconditioning cardioprotection focusing on antioxidant and phase II enzyme induction and their modulation by mitogen activated protein kinases (MAPKs) and phosphatidylinositol 3-kinase (PI3K)/Akt.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
