Wang Sheng, Guo Su-xiang, Dai Zhi-gang, Dong Xi-wei, Liu Yang, Jiang Shan, Wang Zhi-ping
Department of Anesthesiology, Affiliated Hospital of Shihezi Medical School , Shihezi University , Shihezi 832008, China.
Chin Med Sci J. 2011 Mar;26(1):36-42. doi: 10.1016/s1001-9294(11)60017-5.
To test the ability of isoflurane-induced preconditioning against oxygen and glucose deprivation (OGD) injury in vitro.
Rat hippocampal slices were exposed to 1 volume percentage (vol%), 2vol% or 3vol% isoflurane respectively for 20 minutes under normoxic conditions (95% O₂/5% CO₂) once or twice (12 slices in each group) before OGD, with 15-minute washout after each exposure. During OGD experiments, hippocampus slices were bathed with artificial cerebrospinal fluid (ACSF) lacking glucose and perfused with 95% N₂ and 5% CO₂ for 14 minutes, followed by a 30-minute reperfusion in normal ACSF. The CA1 population spike (PS) was measured and used to quantify the degree of neuronal function recovery after OGD. To assess the role of mitogen-activated protein kinases (MAPKs) in isoflurane preconditioning, U0126, an inhibitor of extracellular signal-regulated protein kinase (ERK1/2), and SB203580, an inhibitor of p38 MAPK, were used before two periods of 3vol% isoflurane exposure.
The degree of neuronal function recovery of hippocampal slices exposed to 1vol%, 2vol%, or 3vol% isoflurane once was 41.88%±9.23%, 55.05% ± 11.02%, or 63.18% ± 10.82% respectively. Moreover, neuronal function recovery of hippocampal slices exposed to 1vol%, 2vol%, or 3vol% isoflurane twice was 53.75% ± 12.04%, 63.50% ± 11.06%, or 76.25% ± 12.25%, respectively. Isoflurane preconditioning increased the neuronal function recovery in a dose-dependent manner. U0126 blocked the preconditioning induced by dual exposure to 3vol% isoflurane (6.13% ± 1.56%, P < 0.01) and ERK1/2 activities.
Isoflurane is capable of inducing preconditioning in hippocampal slices in vitro in a dose-dependent manner, and dual exposure to isoflurane with a lower concentration is more effective in triggering preconditioning than a single exposure. Isoflurane-induced neuroprotection might be involved with ERK1/2 activities.
测试异氟烷诱导的预处理对体外氧糖剥夺（OGD）损伤的作用。
在常氧条件（95% O₂/5% CO₂）下，将大鼠海马脑片分别暴露于1体积百分比（vol%）、2vol%或3vol%的异氟烷中20分钟，OGD前进行一次或两次暴露（每组12片脑片），每次暴露后有15分钟的洗脱期。在OGD实验中，海马脑片用无糖的人工脑脊液（ACSF）孵育，并用95% N₂和5% CO₂灌注14分钟，随后在正常ACSF中再灌注30分钟。测量CA1群体峰电位（PS），并用于量化OGD后神经元功能恢复的程度。为评估丝裂原活化蛋白激酶（MAPKs）在异氟烷预处理中的作用，在两次3vol%异氟烷暴露前使用细胞外信号调节蛋白激酶（ERK1/2）抑制剂U0126和p38 MAPK抑制剂SB203580。
一次暴露于1vol%、2vol%或3vol%异氟烷的海马脑片的神经元功能恢复程度分别为41.88%±9.23%、55.05%±11.02%或63.18%±10.82%。此外，两次暴露于1vol%、2vol%或3vol%异氟烷的海马脑片的神经元功能恢复程度分别为53.75%±12.04%、63.50%±11.06%或76.25%±12.25%。异氟烷预处理以剂量依赖的方式增加了神经元功能恢复。U0126阻断了两次暴露于3vol%异氟烷诱导的预处理（6.13%±1.56%，P<0.01）以及ERK1/2活性。
异氟烷能够在体外以剂量依赖的方式诱导海马脑片预处理，且较低浓度的异氟烷两次暴露比单次暴露更有效地触发预处理。异氟烷诱导的神经保护作用可能与ERK1/2活性有关。
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