期刊文献+

补肾活血方对老年性痴呆模型大鼠的治疗作用研究 被引量:1

Therapeutic effect study of bushen huoxue formula on the experimental model of alzheimer's disease
暂未订购
导出
摘要 目的观察补肾活血方对Aβ联合D-半乳糖诱导大鼠老年性痴呆动物模型认知功能的干预作用及其机制。方法脑立体定位仪双侧海马内一次性脑内注射Aβ25-35联合长期颈部皮下注射D-半乳糖制作大鼠AD动物模型,注射24h后灌胃给药,连续4周,以Morris水迷宫实验进行认知行为学检测,ELISA法测定脑组织中SOD、MDA含量。结果补肾活血方组大鼠在安全岛象限的搜索时间和搜索距离较模型组大鼠明显延长。补肾活血方还可降低大鼠脑组织MDA含量,升高SOD活性水平。结论补肾活血方可明显改善Aβ联合D-半乳糖诱导的AD大鼠的学习记忆能力,其作用可能与调节脑内脂质过氧化物反应有关。 Objective To observe the therapeutic effect of Bushen huoxue formula to experimental animal model of Alzheimer's disease.Methods established AD animal model with Aβ25-35 encephalic injection once and D-galactose hypodermical injection for 5 weeks,then administrated the rats with drugs for 4 weeks,after that,check the cognitive behavior with Morris mater maze experiment,and survey the contents of SOD and MDA of the brains.Results After administrated the animal with Bushen huoxue formula,the searching time and distance in safety island quadrant were lengthened.The formula also diminished the content of MDA and elevated the activity of SOD.Conclusion Bushen huoxue formula obviously improved the learning and memonic capacity of AD rats,its mechanism may has certain relationship to its regulating lipid peroxidation reaction effect.
出处 《中国医药科学》 2012年第4期32-33,38,共3页 China Medicine And Pharmacy
基金 国家国际科技合作项目(2010DFB33260)
关键词 AΒ25-35 D-半乳糖 补肾活血方 MORRIS水迷宫 跳台试验 老年性痴呆 Aβ25-35 D-galactose Bushen huoxue formula Morris water maze Step down test Alzheimer's disease
  • 相关文献

参考文献6

二级参考文献30

  • 1王爱萍,史明仪,费文勇,彭爱军.补充银杏外种皮多糖对D-半乳糖致衰老小鼠运动能力的影响[J].中国运动医学杂志,2004,23(6):695-697. 被引量:9
  • 2孙永馨,贾建平,Sabina Janciauskiene.α_1-抗糜蛋白酶对类淀粉样蛋白Aβ_(1-42)诱导细胞表达核转录因子的影响[J].中华神经科杂志,2005,38(2):82-86. 被引量:3
  • 3孙永馨,贾建平,Sabina Janciauskiene.阿尔茨海默病发病与淀粉样β蛋白1~42/α1-抗糜蛋白酶复合物及脂质代谢紊乱的关系[J].中国临床康复,2005,9(9):42-45. 被引量:7
  • 4McGeer PL,McGeer EG.The inflammatory response system of brain:implications for therapy of Alzheimer and other neurodegenerative diseases[J].Brain Res Brain Res Rev,1995,21(2):195-218.
  • 5Potter H,Wefes IM,Nilsson LN.The inflammation-induced pathological chaperones ACT and apo-E are necessary catalysts of Alzheimer amyloid formation[J].Neurobiol Aging,2001,22(6):923-930.
  • 6Nilsson LN,Arendash GW,Leighty RE,et al.Cognitive impairment in PDAPP mice depends on ApoE and ACT-catalyzed amyloid formation[J].Neurobiol Aging,2004,25(9):1153-1167.
  • 7Padmanabhan J,Levy M,Dickson DW,et al.Alphal-antichymotrypsin,an inflammatory protein overexpressed in Alzheimer's disease brain,induces tau phosphorylation in neurons[J].Brain,2006,129(11):3020-3034.
  • 8Baker C,Nielsen HM,Minthon L,et al.Effects of Alzheimer's peptide and a1-antichymotrypsin on astrocyte gene expression[J].Neurobiol Aging,2007,28(1):56-61.
  • 9Eriksson S,Janciauskiene S,Lannfelt L.α1-antichymotrypsin regulates Alzheimer β-amyloid peptide fibril formation[J].Proc Nat Acad Sci USA,1995,92(6):2313-2317.
  • 10Janciauskiene S,Rubin H,Lukacs CM,et al.Alzheimer's peptide Ab1-42 binds to two β-sheets of a1-antichymotrypsin and transforms it from inhibitor to substrate[J].J Biol Chem,1998,273(43):28360-28364.

共引文献23

同被引文献23

引证文献1

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部