Effectof monosialoganglioside on hippocampal Akt/GSK-3β signaling pathway in rats undergoing cardiopulmonary bypass / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of monosialoganglioside (GM-1) on hippocampal protein kinase B (Akt) /glycogen synthase kinase 3β (GSK-3β) signaling pathway in the rats undergoing cardiopulmonary bypass (CPB).Methods Eighteen healthy male Sprague-Dawley rats, aged 6 months, weighing 400-500 g, were randomly divided into 3 groups (n =6 each) using a random number table:control group (group C), CPB group and GM-1 group.GM-1 20 mg/kg was added to the priming solution in group GM-1, while the equal volume of normal saline was given in group CPB.At 3 h after termination of CPB, blood samples were taken from the jugular vein for determination of plasma neuron-specific enolase (NSE) and S-100β protein concentrations using enzyme-linked immunosorbent assay.After blood sampling, the rats were sacrificed, and the hippocampi were isolated for microscopic examination of the ultrastructure of the hippocampal neurons (with electron microscope), and for detection of neuronal apoptosis (with light microscope) and phosphorylation of Akt and GSK-3β (by Western blot).Results Compared with group C, the concentrations of plasma NSE and S-100β protein, and the number of apoptotic neurons were significantly increased in CPB and GM-1 groups, the phosphorylation of Akt and GSK-3β was decreased in group CPB, and the phosphorylation of Akt and GSK-3β was increased in group GM-1 (P＜0.05).Compared with group CPB, the concentrations of plasma NSE and S-100β protein, and the number of apoptotic neurons were significantly decreased, the phosphorylation of Akt and GSK-3β was increased (P＜0.05), and the pathological changes were reduced in group GM-1.Conclusion GM-1 can reduce apoptosis in hippocampal neurons through activating Akt/GSK-3β signaling pathway, thus mitigating CPB-induced brain injury in rats.