bFGF attenuates endoplasmic reticulum stress and mitochondrial injury on myocardial ischaemia/reperfusion via activation of PI 3K/Akt/ ERK 1/2 pathway

Extensive research focused on finding effective strategies to prevent or improve recovery from myocardial ischaemia/reperfusion (I/R) injury. Basic fibroblast growth factor (b FGF ) has been shown to have therapeutic potential in some heart disorders, including ischaemic injury. In this study, we demonstrate that b FGF administration can inhibit the endoplasmic reticulum ( ER ) stress and mitochondrial dysfunction induced in the heart in a mouse model of I/R injury. In vitro , b FGF exerts a protective effect by inhibiting the ER stress response and mitochondrial dysfunction proteins that are induced by tert‐Butyl hydroperoxide ( TBHP ) treatment. Both of these in vivo and in vitro effects are related to the activation of two downstream signalling pathways, PI3K/Akt and ERK 1/2. Inhibition of these PI3K/Akt and ERK 1/2 pathways by specific inhibitors, LY294002 and PD98059, partially reduces the protective effect of b FGF . Taken together, our results indicate that the cardioprotective role of b FGF involves the suppression of ER stress and mitochondrial dysfunction in ischaemic oxidative damage models and oxidative stress‐induced H9C2 cell injury; furthermore, these effects underlie the activation of the PI3K/Akt and ERK 1/2 signalling pathways.