Effects of propofol and sevoflurane anesthesia on cognitive function and amyloid beta protein deposition in hippocampi of aged mice

Objective To evaluate the effects of propofol and sevoflurane anesthesia on cognitive function and amyloid beta protein (Aβ) deposition in hippocampi of aged mice. Methods Thirty-six SAMP8 mice, aged 6 months, weighing 29-32 g, were randomly assigned into 4 groups (n=9 each) using a random number table: control group (group C) , propofol anesthesia group (group P) , sevoflurane anesthesia group (group S) and propofol plus sevoflurane anesthesia group (group PS) . In group P, propofol 140 mg/kg was injected intraperitoneally, when righting reflex occurred, additional propofol 70 mg/kg was given, and when it occurred again, additional propofol 40 mg/kg was given.Group S continuously inhaled 1% sevoflurane for 120 min.Group PS continuously inhaled 2% sevoflurane for 120 min, and when righting reflex occurred, additional propofol 40 mg/kg was given.Anesthesia was maintained for 120 min in P, S and PS groups.Before anesthesia and at 7, 14 and 28 days after anesthesia, Morris water maze test was performed, and the escape latency was recorded.Hippocampi were obtained to determine the expression of Aβ using immuno-histochemistry. Results Compared with group C, the escape latency was significantly prolonged at 7 days after anesthesia, and the expression of Aβ was up-regulated at 7, 14 and 28 days after anesthesia in group S, and no significant change was found in the parameters mentioned above in P and PS groups.Compared with the value at 7 days after anesthesia, the expression of Aβ was significantly down-regulated at 14 and 28 days after anesthesia in group S, and no significant change was found in the expression of Aβ at 14 and 28 days after anesthesia in C, P and PS groups. Conclusion Although sevoflurane anesthesia promotes Aβ deposition in hippocampi, it only causes short-term cognitive dysfunction, however, anesthesia with propofol or with propofol in combination with sevoflurane produces no influence in aged mice. Key words: Anesthetics, inhalation; Propofol; Amyloid beta-protein; Hippocampus; Cognition; Aged