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.
出处
《世界临床药物》
CAS
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)
