期刊文献+

姜黄素对APPswe/PSEN1dE9双转基因小鼠海马神经元SR-BⅠ和ABCA1表达的影响 被引量:1

Effects of curcumin on the expression of SR-BⅠ and ABCA1 in neurons of hippocampus of APPswe/PSEN1dE9 double transgenic mice
下载PDF
导出
摘要 目的:观察姜黄素对β-淀粉样前体蛋白swe基因/早老蛋白1dE9基因(APPswe/PSEN1dE9)双转基因小鼠海马神经元B类Ⅰ型清道夫受体(scavenger receptor class B typeⅠ,SR-BⅠ)和三磷酸腺苷结合盒A1(ATP-binding cassette transporter,ABCA1)表达的影响,探讨姜黄素在阿尔茨海默病(Alzheimer’s disease,AD)防治中的机制。方法:将10只6月龄的APPswe/PSEN1dE9双转基因小鼠随机分为对照组和姜黄素饲喂组,每组5只。姜黄素饲喂组每天饲喂500 ppm姜黄素,6个月后采用免疫组化法检测小鼠海马神经元SR-BⅠ和ABCA1表达的变化。结果:与对照组相比,姜黄素饲喂组小鼠海马神经元ABCA1表达明显增加(t=-10.805,P=0.000),但2组小鼠海马神经元中均未见SR-BⅠ表达。结论:姜黄素能提高APPswe/PSEN1dE9双转基因小鼠海马神经元ABCA1的表达,而SR-BⅠ在神经元中未见表达。 Objective :To observe the effect of curcumin on expression of scavenger receptor class B type I (SR-B I ) and ATP-bind- ing cassette transporter 1 (ABCA1) in neurons of hippocampus of APPswe/PSENldE9 double transgenic mice and to investigate the mechanism of curcumin in the prevention and treatment of Alzheimer's disease. Methods:Ten six-month-old APPswe/PSEN l dE9 double transgenic mice were randomly divided into control group and curcumin group. Each group had 5 mice. Mice in curcumin group were fed curcumin 500 ppm every day. Six months later,changes of the expression of SR-B I and ABCA1 in neurons of hippicampus were detected by immunohistochemistry. Results :Expression of ABCA1 in neurons of hippocampus of mice in curcumin group was increased significantly compared with that of control group (t=-10.805,P=0.000) while expression of SR-B I was not detected in both groups. Conclusions:Curcumin can induce expression of ABCA1 in neurons of hippoeampus of APPswe/PSENldE9 double transgenie mice while expressions of SR-B I can not be detected in neurons.
出处 《重庆医科大学学报》 CAS CSCD 北大核心 2014年第2期141-145,共5页 Journal of Chongqing Medical University
基金 国家自然科学基金资助项目(编号:81271426、30973154、81100948)
关键词 姜黄素 β-淀粉样前体蛋白swe基因 早老蛋白1dE9基因双转基因小鼠 海马 B类Ⅰ型清道夫受体 三磷酸腺苷结合盒A1 curcumin APPswe/PSEN 1 dE9 double transgenic mice hippocampus scavenger receptor class B type I ATP-binding cas-sette transporter 1
  • 相关文献

参考文献34

  • 1Reitz C,Brayne C,Mayeux R.Epidemiology of Alzheimer disease[J]. Nat Rev Neurol,2011,7(3) : 137-152.
  • 2Walsh DM,Teplow DB.Alzheimer's disease and the amyloid 13-pro- tein[J].Prog Mol Biol Transl Sci,2012,107:101-124.
  • 3Thanopoulou K,Fragkouli A,Stylianopoulou F,et al.Scavenger re- ceptor class B type I (SR-B I ) regulates perivascular macrophages and modifies amyloid pathology in an Alzheimer mouse model[J].Proc Natl Acad Sci USA,2010,107(48) :20816-20821.
  • 4Kim WS, Rahmanto AS, Kamili A,et al.Role of ABCG1 and ABCA 1 in regulation of neuronal cholesterol efflux to apolipoprotein E discs and suppression of amyloid-beta peptide generation[J].J Biol Chem, 2007,282 (5) : 2851-2861.
  • 5Zhang X,Yin WK,Shi XD,et al.Curcumin activates Wnt/13-catenin signaling pathway through inhibiting the activity of GSK-313 in APPswe transfected SY5Y cells[J].Eur J Pharm Sci, 2011,42 (5) : 540-546.
  • 6Ono K,Hasegawa K,Naiki H,et al.Curcumin has potent anti-amy- loidogenic effects for Alzheimer's beta-amyloid fibrils in vitro[J].J Neu- rosci Res, 2004,75 (6) : 742-750.
  • 7Peschel D,Koerting R,Nass N.Curcumin induces changes in ex- pression of genes involved in cholesterol homeostasis[J].J Nutr Biochem, 2007,18(2) : 113-119.
  • 8Dong SZ,Zhao SP,Wu ZH,et al.Curcumin promotes cholesterol ef- flux from adipocytes related to PPARgamma-LXRalpha-ABCA1 pass- way[J].Mol Cell Biochem, 2011,358 (1-2) : 281-285.
  • 9Vaya J, Schipper HM. Oxysterols, cholesterol homeostasis, and Alzheimer disease[J].J Neurochem, 2007,102 (6) : 1727-1737.
  • 10Pfrieger FW,Ungerer N.Cholestero! metabolism in neurons and as- troeytes[J].Prog Lipid Res, 2011,50(4) : 357-371.

二级参考文献45

  • 1王跃春.Y型电迷宫在大鼠学习记忆功能测试中的合理运用[J].中国行为医学科学,2005,14(1):69-70. 被引量:61
  • 2Winter Y,Korchounov A,Bertschi N E,et al.Depression in elderly patients with alzheimer dementia or vascular dementia and its influence on their quality of life[J].Neurosci Rural Pract, 2011,2 ( 1 ):27-32.
  • 3Lee J S,Im D S,An Y S,et al.Chronic cerebral hypoperfusion in a mouse model of Alzheimer's disease:an additional contributing factor of cognitive impairment[J].Neurosci Lett, 201l, 489 (2) : 84-88.
  • 4Brown W R,Thore C R.Review:cerebral microvascular pathology in ageing and neurodegeneration[J].Neuropathol Appl Neurobiol,2011, 37(1 ) :56-74.
  • 5Sarti C,Pantoni L, Bartolini L, et al.Cognitive impairment and ehronie eerebral hypoperfusion:what ean be learned from experimental models[J].Neurol Sei, 2002,203 : 263-266.
  • 6Cechetti F,Pagnussat A S,Worm P V,et al.Chronic brain hypoper- fusion causes early glial activation and neuronal death,and subsequent long-term memory impairment[J].Brain Res Bull,2012,87( 1 ):109-116.
  • 7Farkas E,Luiten P G,Bari F.Permanent,bilateral common carotid artery occlusion in the rat:a model for chronic cerebral hypoperfusion- related neurodegenerative diseases[J].Brain Res Rev, 2007,54 ( 1 ) : 162- 180.
  • 8Cechetti F,Worm P V,Pereira L O,et al.The modified 2VO is- chemia protocol causes cognitive impairment similar to that induced by the standard method,but with a better survival rate[J].Braz J Med Biol Res, 2010,43(12) : 1178-1183.
  • 9Dietschy J M,Turley S D.Cholesterol metabolism in the brain[J]. Curr Opin Lipido1,2001,12(2) : 105-112.
  • 10Korade Z,Kenworthy A K.Lipid rafts,cholesterol,and the brain[J]. Neuropharmacology, 2008,55 (8) : 1265-1273.

共引文献9

同被引文献16

引证文献1

二级引证文献1

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