PI3K/Akt/FoxO3a signaling mediates cardioprotection of FGF-2 against hydrogen peroxide-induced apoptosis in H9c2 cells

摘要: Cardiovascular disease is a growing major global public health problem. Oxidative stress regarded as one of the key regulators pathological physiology, which eventually leads to cardiovascular disease. However, mechanisms by FGF-2 rescues cells from oxidative damage in not fully elucidated. Herein this study was designed investigate protective effects H2O2-induced apoptosis H9c2 cardiomyocytes, well possible signaling pathway involved. Apoptosis cardiomyocytes induced H2O2 and assessed using methyl thiazolyl tetrazolium assay, Hoechst, TUNEL staining. Cells were pretreated with PI3K/Akt inhibitor LY294002 pathways involved protection FGF-2. The levels p-Akt, p-FoxO3a, Bim detected immunoblotting. Stimulation decreased phosphorylation Akt FoxO3a, nuclear localization FoxO3a cells. These abrogated pretreatment Furthermore, abolished LY294002. In conclusion, our data suggest that protects against via activation PI3K/Akt/FoxO3a pathway.