摘要
Background Granulocyte-macrophage colony-stimulating factor （GM-CSF） is a potent hematopoietic growth factor that both enhances the survival and drives the differentiation and proliferation of myeloid lineage cells. Recent studies have suggested that GM-CSF has a neuroprotective effect against cerebral ischemia injury, but the molecular mechanisms have been unclear. This study aimed to investigate the influences of a short-acting （half-life 3.5 hours） G-CSF and a long-acting （half-life 40 hours） pegylated G-CSF on the JNK signaling pathway after cerebral ischemia reperfusion.
Background Granulocyte-macrophage colony-stimulating factor （GM-CSF） is a potent hematopoietic growth factor that both enhances the survival and drives the differentiation and proliferation of myeloid lineage cells. Recent studies have suggested that GM-CSF has a neuroprotective effect against cerebral ischemia injury, but the molecular mechanisms have been unclear. This study aimed to investigate the influences of a short-acting （half-life 3.5 hours） G-CSF and a long-acting （half-life 40 hours） pegylated G-CSF on the JNK signaling pathway after cerebral ischemia reperfusion.
