首页> 中文期刊> 《中华麻醉学杂志》 >七氟醚麻醉对淀粉样前蛋白转基因小鼠认知功能及海马神经元Tau蛋白磷酸化水平的影响

七氟醚麻醉对淀粉样前蛋白转基因小鼠认知功能及海马神经元Tau蛋白磷酸化水平的影响

         

摘要

Objective To investigate the effect of sevoflurane anaesthesia on the cognitive function and phosphorylation of tau protein in hippocampal neurons in amyloid precursor protein (APP) transgenic mice.Methods Male APP gene mutation mice,weighing 18-22 g and aged 8-12 weeks,were used in this study.Forty-four APP positive mice were randomly divided into two groups:sevoflurane group (group AS,n =28) and control group (group AC,n =16).And other forty-four APP negative mice were randomly divided into two groups:sevoflurane group (group S,n =28) and control group (group C,n =16).The animals in groups S and AS inhaled 3% sevoflurane for 4 hours.While in groups C and AC,the animals inhaled pure oxygen for 4 hours.Morris water maze was performed 24 hours after sevoflurane or pure oxygen inhalation.The phosphorylation of tau protein at Ser262 and Ser396 sites was detected by Western blotting on 1 day after pure oxygen inhalation in groups AC and C,and on 1,3 and 7 days after sevoflurane inhalation in groups AS and S.Results Compared with group C,the escape latency was significantly prolonged and the duration of staying at the original platform quadrant was shortened in groups S and AC,and the phosphorylation of tau protein at Ser262 site in group S and phosphorylation of tau protein at Ser262 and Ser396 sites in group AS were increased (P < 0.05).Compared with group S,the escape latency was significantly prolonged,the duration of staying at the original platform quadrant was shortened,and the phosphorylation of tau protein at Ser262 and Ser396 sites was increased in group AS (P < 0.05).Compared with group AC,the escape latency was significantly prolonged,the duration of staying at the original platform quadrant was shortened,and the phosphorylation of tau protein at Ser262 and Ser396 sites was increased in group AS (P<0.05).Conclusion Sevoflurane anesthesia can aggravate the impairment of cognitive function in APP positive mice and the increase in the phosphorylation of tau protein at Ser262 and Ser396 sites is involved in the mechanism.

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