Abstract

Objective To investigate the mechanism by which Propofol alleviates Ketamine anesthesia induced injury in hippocampal neurons and cognitive function of young rats. Methods Eighty 7- day- old SD rats were randomly divided into the normal saline (NS) group, Ketamine 70 mg/kg group (K group) , Ketamine 70 mg/kg+Propofol 35 mg/kg (P+K low dose) group, Ketamine 70 mg/kg+Propofol 70 mg/kg (P+ K high dose) group (n=20 each). All rats received 1 mL corresponding drugs via intraperitoneal injection, with the 2 h dosing interval, and maintained for 6 h. After anesthesia, 10 rats in each group were randomly selected and executed. The hippocampal tissues from the rats were taken for section. The hippocampal CA1 neuronal cell apoptosis, hippocampal CA1 cysteinyl aspartate - specific proteinases - 3 (Caspace-3) protein, hippocampal neurons threonine 231 site phosphorylation tau protein (Tau-pThr231) , and serine 4.4 site phosphorylation tau protein (Tau- pSer404) expression were measured. The remaining young rats in each group were fed for 21 d, then underwent water maze test. Results Compared with the P+ K low dose group, P+K high dose group and NS group, the latency time at 3 d in the K group (98.64±15.63 vs 81.26±5.69, 64.17±4.26, 51.97±13.26) was increased (P 0.05). There was no significant difference in ther hippocampal neurons Tau - pSer404 protein expression among the four groups (P>0.05). Conclusion Propofol can reduce Ketamine anesthesia induced injury in hippocampal neurons and cognitive function of young SD rats. Its mechanism may be inhibiting the up- regulation of Caspace- 3 protein expression and Tau phosphorylation, and reducing neuronal apoptosis. Key words: Hippocampus; Propofol; Ketamine; Cognitive function

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