Objective To investigate the ability of once and twice isoflurane preconditioning against oxygen and glucose deprivation（OGD） injury in rats brain in vitro.Methods Rat hippocampal slices were exposed to 1vol%,2vol% and 3vol% isoflurane for 30 min under normoxic condition（95% O2/5% CO2） once and twice（n=12 for each group） respectively before OGD.At the end of each exposure,the slices were set with a 15-min washout period interspersed,then slices were exposed to 13-min OGD period（95% N2/5%CO2,glucose-free） followed by 30min reoxygenation.The amplitude CA1 population spikes（PS,neuronal function） was measured and used to quantify the degree of recovery of neuronal function at post OGD period.To assess the role of the mitogen-activated protein kinases（MAPKs） in preconditioning,U0126,an inhibitor of extracellular signal-regulated protein kinase（MEK-ERK1/2）,and SB203580,an inhibitor of p38 MAPK,were used during isoflurane exposure.Results Isoflurane-preconditioning with 1vol%,2vol% and 3vol% once increased the degree of recovery from 4.8%±1.4%（control） to 41.9%±9.2%,55.1%±11.0% and 63.2%±10.8%,respectively,and twice to 53.8%±12.0%,63.5%±11.1% and 76.3%±12.3%, respectively.The effect of twice exposure to 3vol% isoflurane was blocked by U0126（6.1%±1.5%）.Conclusion It is concluded that twice isoflurane preconditioning could achieve better neuroprotection than once via activation of extracellular signal-regulated protein kinase（MEK-ERK1/2）.
目的观察盐酸度洛西汀对糖尿病神经病理痛大鼠脊髓背角星形胶质细胞和小胶质细胞的影响。方法将30只SD大鼠随机分为3组:对照组(C ontrol组),模型组(D N P组),盐酸度洛西汀组(D LX组)各10只。链脲佐菌素(ST Z)注射前1 d及注射后7,14,21,28 d测定大鼠机械缩足阈值(M W T)和热缩足潜伏期(T W L)。D LX组于ST Z注射15 d起腹腔注射10 m g/kg盐酸度洛西汀,连续14 d,并于14,21,28 d测定W M T和T W L。行为学检测完成后选择28 d大鼠用免疫荧光法、蛋白印迹法测定脊髓背角G FA P、iba-1的表达。结果造模前大鼠M W T、T W L无明显差异(P>0.05)。造模后D N P组、D LX组较C ontrol组M W T降低、T W L缩短(P<0.05),且G FA P与iba-1的表达较C ontrol组上调(P<0.05);腹腔注射度洛西汀后,与D N P组比较,D LX组M W T升高,T W L延长,且G FA P与iba-1表达下调(P<0.05)。结论盐酸度洛西汀能明显减轻糖尿病大鼠神经病理性疼痛,其机制可能与抑制星形胶质细胞和小胶质细胞的表达有关。
