Effects of sevoflurane on β-amyloid-induced cognitive dysfunction and oxidative stress response of hippocampal tissues in rats

Objective To evaluate the effects of sevoflurane on β-amyloid (Aβ)-induced cognitive dysfunction and oxidative stress response of hippocampal tissues in rats.Methods Ninety-six male adlut SpragueDawley rats,weighing 250-300 g,were randomly divided into 4 groups (n =24 each) using a random number table:control group (group C) ; group Aβ ; 1.3 ％ sevoflurane group (group S1) and 2.6 ％ sevoflurane group (group S2).The animals were anesthetized with intraperitoneal.10％ chloral hydrate 350 mg/kg.Cognitive dysfunction was induced by injecting Aβ1-40 2 μ1 into the bilateral hippocampi in Aβ,S1 and S2 groups.The equal volume of normal saline was given in group C.At 22 days after injection,C and Aβ groups were exposed to 30％ oxygen for 4 h,and S1 and S2 groups inhaled 1.3 ％ and 2.6 ％ sevoflurane,respectively,for 4 h.Eight rats were chosen at days 1,3 and 7 after exposure and cognitive function was assessed by Morris water maze test.The swimming speed,escape latency and exploration time at the original platform quadrant were recorded.The rats were then sacrificed after the end of the behavioral test and blood samples were taken for determination of serum S100β protein concentration.Hippocampi were immediately isolated and the homogenate was prepared for determination of superoxide dismutase (SOD) activity and malondialdehyde (MDA) content.Results Compared with group C,the escape latency was significantly prolonged and exploration time at the original platform quadrant was shortened,the serum S100β protein concentration and MDA content were increased,and SOD activity was decreased at each time point in group Aβ (P ＜ 0.05).There were no significant differences in the variables mentioned above between Aβ and S1 groups (P ＞ 0.05).The escape latency was significantly prolonged and the exploration time at the original platform quadrant was shortened,the serum S100β protein concentration and MDA content were increased,and SOD activity was decreased at each time point in group S2 as compared with Aβ and S1 groups (P ＜ 0.05).There was no significant difference in the swimining speed among the 4 groups (P ＞ 0.05).Conclusion Inhalation of 2.6 ％ sevoflurane for 4 h can aggravate the cognitive dysfunction induced by Aβ in rats and aggravation of oxidative stress response may be involved in the mechanism. Key words: Anesthetics, inhalation ;  Amyloid ;  Cognition disorders ;  Oxidative stress