Ｏｂｊｅｃｔｉｖｅ　To investigate the effect of monosialotetrahexosylganglioside（GM-1） on cardiopulmonary bypass （CPB）-associated brain injury and extrallular signal regulated protein kinase （ERK1/2） signaling pathway.　Methods　Twenty-seven adult male SD rats weighing 350 g-450 g were randomly divided into 3 groups（group S, group B, group C, n=9）： xperimental model of CPB in rats was established via left carotid and right jugular vein cannulation for arterial perfusion and venous return respectively. CPB model was not made in the control group（group S）. Saline（1 mg/kg） was administrated for priming fliud in group B. GM-1（20 mg/kg） was administrated for priming fliud in group C. CPB was maintained for 60 min in group B and C. MAP and blood gas analysis were recorded prior to CPB（T0）， CPB immediately（T1）， CPB 15 min（T2）， CPB 45 min（T3）， 1 h after CPB（T4）. Brain samples were collected at 3 h after CPB. Electron microscopy technique was used to observe ultrastructure of the cerebral cortex， ERK1/2 were detected by immunohistochemistry and neuron apoptosis were quantitatively examined with terminal dexynucleotidyl transferase（TdT）-mediated dUTP nick end labeling（TUNEL） method， ERK1/2 protein activity was detected by Western-blot.　Results　There were no statistically difference between group B and group C in mean arterial pressure， heart rate， partial pressure of oxygen， carbon dioxide partial pressure or hematocrit during CPB. Compared with group S， the ultrastructural changes obviously under the transmission electron microscope， the apoptosis nerve cells of hippocampus were significantly increased （220% and 147%，P<0.05， respectively）， and the expression of ERK1/2 protein were also statistically increased（65% and 41%， P<0.05， respectively） in group B and group C. Compared with group B， the ultrastructural changes was significantly less. The apoptosis nerve cells of hippocampus were significantly reduced（24%， P<0.05）， the expression of ERK1/2 protein was statistically decreased（15%，P<0.05） in group C.　Conclusions　GM-1 plays an important role in protection of CPB- associated cerebral injury. It may due to inhibit ERK1/2 signaling pathway related neuronal apoptosis.