Zhang Yan, Tian Shou-Yuan, Li Yan-Wei, Zhang Ling, Yu Jian-Bo, Li Jing, Chen Yi-Yang, Wang Ya-Xin, Liang Yu, Zhang Xiu-Shan, Wang Wen-Sheng, Liu Hai-Gen
Department of Anesthesiology, Tianjin Huanhu Hospital, Tianjin Neurosurgery Institute, Tianjin 300060, China.
Department of Anesthesiology, The First Hospital Affiliated Shanxi Medical University, Taiyuan, Shanxi 030001, China.
Gene. 2015 Sep 10;569(1):60-5. doi: 10.1016/j.gene.2015.05.026. Epub 2015 May 13.
In this study, we aimed to assess the neuroprotective effect of sevoflurane preconditioning in a cerebral focal ischemia-reperfusion rat model. Sixty Sprague Dawley rats were divided into six groups: sham operated group, cerebral focal ischemia-reperfusion (CIR) group, CIR+sevoflurane preconditioning (SP) (2%) group, CIR+sevoflurane preconditioning (2.5%) group, CIR+sevoflurane preconditioning (3%) group, and CIR+sevoflurane preconditioning (3.5%) group. All subjects were euthanized 2days post-surgery and their hippocampus tissues were removed. Tissue malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) and glutathione peroxidase (GSH-Px) levels were measured and hippocampus tissue samples were examined histopathologically. Results showed that significant difference in antioxidant, immunity indexes, and apoptosis-related protein expression was detected in hippocampus tissue between sham-operated control and CIR groups. Sevoflurane preconditioning significantly dose-dependently reduced MDA, IL-1β, IL-6, IL-10 and TNF-α levels and enhanced antioxidant enzyme activities in hippocampus tissue of CIR+SP groups compared to CIR group. In addition, sevoflurane preconditioning significantly dose-dependently upregulated PI3K, p-Akt and Bcl-2 levels and downregulated caspase-3 and Bax levels in hippocampus tissue of CIR+SP groups compared to CIR group. It can be concluded that sevoflurane preconditioning demonstrates a strong and ameliorative effect on cerebral I/R damage in rats. The neuroprotective mechanisms of sevoflurane preconditioning are associated with its properties of anti-apoptosis and anti-oxidation as well as regulation of PI3K and p-Akt signal activation.
在本研究中，我们旨在评估七氟醚预处理对大鼠局灶性脑缺血再灌注模型的神经保护作用。将60只Sprague Dawley大鼠分为六组：假手术组、局灶性脑缺血再灌注（CIR）组、CIR+七氟醚预处理（SP）（2%）组、CIR+七氟醚预处理（2.5%）组、CIR+七氟醚预处理（3%）组和CIR+七氟醚预处理（3.5%）组。所有实验对象均在术后2天安乐死，并取出其海马组织。测量组织丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽（GSH）和谷胱甘肽过氧化物酶（GSH-Px）水平，并对海马组织样本进行组织病理学检查。结果显示，假手术对照组和CIR组之间的海马组织在抗氧化、免疫指标和凋亡相关蛋白表达方面存在显著差异。与CIR组相比，七氟醚预处理显著剂量依赖性地降低了CIR+SP组海马组织中的MDA、IL-1β、IL-6、IL-10和TNF-α水平，并增强了抗氧化酶活性。此外，与CIR组相比，七氟醚预处理显著剂量依赖性地上调了CIR+SP组海马组织中的PI3K、p-Akt和Bcl-2水平，并下调了caspase-3和Bax水平。可以得出结论，七氟醚预处理对大鼠脑缺血再灌注损伤具有强大的改善作用。七氟醚预处理的神经保护机制与其抗凋亡、抗氧化特性以及对PI3K和p-Akt信号激活的调节有关。
