Objective To explore the effects of sevoflurane on learning-memory and the signaling pathway of phosphatidylinositol -3- excitation enzyme (PI3K) / protein kinase B / (AKT) in juvenile rats,in order to provide theoretical evidence for related research . Method Totally 36 juvenile male SD rats (8 weeks old,220~250 g) were randomly divided into control group and experimental group using random number table.And the control group was divided into two subgroups:the vacuity contrast group (CON group) where rats were not treated and the positive control group (O2 group) where rats inhaled pure oxygen for 30 minutes.The rats in the experimental group inhaled 2% sevoflurane for 30 minutes,and were divided into 4 subgroups:revive 2 h after anesthesia (T1 group),12 h (T2 group),24 h group (T3 group) and 72 h group (T4 group),with 6 rats in each group.All rats were trained by Morris water maze before anaesthesia.After anaesthesia,the Morris water maze behavior test was carried out again at every time point.The expression of PI3K mRNA and AKT mRNA in hippocampus of rats were detected by PCR method. Results There was no statistical difference in the behavior of rats in each group before anesthesia (P>0.05).Compared with the O2 group,the escape latency after anesthesia was significantly prolonged in T1 group(P<0.05).Compared with the T1 group,the escape latency was shortened in T3 and T4 group(both P<0.05).There was no significant difference on the total route among each group (P>0.05).Compared with CON group,the expression of PI3K mRNA and AKT mRNA in O2 group were significantly up-regulated,while the expression of PI3K mRNA and AKT mRNA in the T1 group were markedly down-regulated (all P<0.05).Compared with O2 group,the expression of PI3K mRNA and AKT mRNA in T1 group significantly decreased (both P<0.05). Conclusions Sevoflurane anesthesia can cause temporary cognitive dysfunction in juvenile rats.And the mechanism is related to the inhibition of the expression of PI3K/AKT signaling pathway.
Key words
sevoflurane /
learning-memory /
signal pathway /
PI3K/ AKT
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References
[1] Zhang DX, Jiang S,Yu LN ,et al.The effect of sevoflurane on the cognitive function of rats and its association with the inhibition of synaptic transmission[J].Int J Clin Exp Med,2015,8(11):20853-20860.
[2] 陈筱诗,杨进国.七氟醚对发育期大脑毒性作用的研究进展[J].临床麻醉学杂志,2017,33(11):1141-1144.
[3] Xia Y,Xu H,Jia C,et al.Tanshinone IIA attenuates sevoflurane neurotoxicity in neonatal mice[J].Anesth Analg,2017,124(4):1244-1252.
[4] Guo RT,Yan L,Qing SX,et al.Docosahexaenoic acid rescues synaptogenesis impairment and long-term memory deficits caused by postnatal multiple sevoflurane exposures[J].Biomed Res Int,2016,2016:4062579.
[5] Hu N,Guo D,Wang H,et al.Involvement of the blood—brain barrier opening in cognitive decline in aged rats following orthope-die surgery and high concentration of sevoflurane inhalation[J].Brain Res,2014,1551:13-24.
[6] 郑雪,朱昭琼,张超,等.异氟醚对大鼠S100、Tau和β淀粉样蛋白的影响[J].临床麻醉学杂志,2013,29(9):911-913.
[7] Lai Z,Zhang L,Su J,et al.Sevoflurane post conditioning improves long-term learning and memory of neonatal hypoxia-ischemia brain damage rats via the PI3K/Akt-mPTP pathway[J].Brain Res,2016,1630:25-37.
[8] 高洋洋,赵志英.PI3K/AKT信号通路及神经损伤的研究进展[J].医学综述,2017,23(16):3121-3125.
[9] 唐春春,王义任,娟娟,等.多次七氟醚麻醉对新生大鼠海马ApoE表达的影响[J].中华麻醉学杂志,2016,36(5):535-538.
[10] Ma H,Yao L,Pang L,et al.Tetrandrine ameliorates sevofluraneinduced Cognitive impairment via the suppression of inflammation and apoptosis in aged rats[J].Mol Med Rep,2016,13(6):4814-4820.
[11] Yang X,Yang S,Hong C,et al.Panax notoginseng saponins attenuates sevoflurane induced nerve cell injury by modulating AKT signaling pathway[J].Mol Med Rep,2017,16(5):7829-7834.
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