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作 者:陈嘉[1] 顾丰华[1] 刘翔[1] 许海燕[1] 杨培明[1] 董文心[1]
机构地区:[1]中国医药工业研究总院上海医药工业研究院创新药物与制药工艺国家重点实验室,上海200437
出 处:《世界临床药物》2013年第1期21-25,40,共6页World Clinical Drug
基 金:2008-2011年上海市中药现代化资助项目(项目编号:08DZ1971802)
摘 要:目的研究SIPI-SCPd是否通过抗氧化作用来改善小鼠的学习记忆功能。方法采用过氧化氢(H2O2)造成体外原代培养的大鼠海马细胞氧化损伤模型。观察高、中和低剂量SIPI-SCPd(20、2和0.2 mg/L)对损伤的大鼠海马细胞的保护作用;通过成年ICR小鼠皮下注射D-半乳糖8周建立老年痴呆症(AD)小鼠模型,并同时给予维生素E及不同剂量SIPI-SCPd(70、35、17.5和8.75 mg/kg),应用Morris水迷宫试验观察不同组小鼠的空间学习记忆能力,并于行为学试验后检测小鼠脑组织MDA含量和SOD活性。结果 20和2 mg/L的SIPI-SCPd可以显著改善H2O2损伤的大鼠海马细胞(P<0.05);在撤台试验中,与模型组相比,35和17.5 mg/kg SIPI-SCPd组小鼠第一次穿越平台的时间降低,穿越平台次数增加,17.5mg/kg组小鼠中心活动路程和站台周围范围Ⅰ路程显著增加(P<0.05),各剂量SIPI-SCPd组小鼠脑内SOD活力有一定程度升高,MDA含量出现降低趋势。结论 SIPI-SCPd具有改善D-半乳糖诱导的AD模型小鼠学习记忆的能力,其机制可能与抗氧化损伤相关。Object To study the effect of SIPI-SCPd on improving learning and memory of dementia mice caused by D-galactose.Methods The oxygen free radical injury model by H2O2 on cultured neonate rat hippocampal neurons was established to evaluate protective effect of SIPI-SCPd with high,medium and low dose(20,2 and 0.2 mg/L) in vitro.The dementia ICR mice caused by D-galactose were treated by SIPI-SCPd with 70,35,17.5 and 8.75 mg/kg(i.g) with Vit-E for 8 weeks.The spatial memory function of mice was tested by Morris water maze,as well as the SOD and MDA were measured in mice brain after the behavioral test.Results SIPI-SCPd with 20 and 2 mg/L could protect cultured neonate rat hippocampal neurons against injury by H2O2.SIPI-SCPd with 35 and 17.5 mg/kg could improve the learning and memory ability of dementia mice by decreasing latency(s) to reach the goal,increasing the frequency of site crossings significantly.SIPI-SCPd with the dose of 17.5 mg/kg increased the path length within space closing to platform in the Morris water maze.SIPI-SCPd could also increase SOD and decrease MDA in the dementia mice brain slightly.Conclusion SIPI-SCPd may be benifit to ameliorate learning and memory ability injured by D-galactose through its antioxygen mode.
关 键 词:SIPI-SCPd D-半乳糖 石菖蒲水提取物 学习记忆
分 类 号:R332[医药卫生—人体生理学] R931.71[医药卫生—基础医学]
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