Hyperosmotic stress-dependent NFκB activation is regulated by reactive oxygen species and IGF-1 in cultured cardiomyocytes

摘要: We have recently shown that hyperosmotic stress activates p65/RelB NFκB in cultured cardiomyocytes with dichotomic actions on caspase activation and cell death. It remains unexplored how is regulated rat exposed to stress. study here: (a) if triggers reactive oxygen species (ROS) generation turn whether they regulate (b) insulin-like growth factor-1 (IGF-1) modulates ROS production hyperosmotically-stressed cardiomyocytes. The results showed generated cardiac myocytes, particular the hydroxyl superoxide species, which were inhibited by N-acetylcysteine (NAC). Hyperosmotic stress-induced as determined IκBα degradation DNA binding. procaspase-3 -9 fragmentation prevented NAC IGF-1. However, this factor did not decrease induced stress, suggesting its over may be due modulation of events downstream generation. conclude induces ROS, caspases. IGF-1 prevents a ROS-independent mechanism.