期刊文献+

海风藤选择性抑制淀粉样前体蛋白基因表达(英文) 被引量:5

Selective inhibition of haifengteng in gene expression of beta-amyloid precursor protein
下载PDF
导出
摘要 背景:淀粉样蛋白(β-amyloidprotein,β-AP)是老年斑的核心成分,它在脑内的沉积与阿尔茨海默病(Alzheimer'sAD)发病有着密切的关系。现代研究证实β-AP来源于淀粉样前体蛋白(β-amyloidprecursorprotein,β-APP),如果β-APP基因表达受到抑制,β-AP在脑内的沉积就会减少,阿尔茨海默病(Alzheimerdisease,AD)有可能得到有效防治。因此,很多国内外学者都在积极寻找β-APP基因表达抑制物,企图发现防治AD的有效药物。目的:研究海风藤对人类神经母细胞瘤细胞β-APP基因表达的影响。设计:药物(海风藤)干扰和非药物干扰对照;目的基因(β-APP)与结构基因(β-Actin)对照。材料:人类神经母细胞瘤细胞系列(SK-N-SH),海风藤。方法:应用细胞培养和反转录—聚合酶链反应(RT-PCR)观察海风藤不同浓度和不同时间对β-APPmRNA的影响。结果:海风藤选择性的抑制β-APP基因表达,这种抑制作用随时间的延长和浓度的增加而增强。结论:海风藤选择性抑制β-APP基因表达,为其防治AD提供了更加可靠的实验依据。 BACKGROUND:Beta-amyloid protein(β-AP) is a core element in senile plague an d its cerebral deposition closely relates to the onset of Alzheimer's disease(AD ).Modern researches prove that β-AP is originated form beta-amyloid precursor protein(β-APP).If the gene expression of β-APP can be inhibited,the cerebra l deposition of β-AP will decrease,and therefore,AD might be treated effective ly.Hence,many national and international scholars are actively searching for the inhibitors that could inhibit the gene expression of β-APP for effective medi cations in AD treatment. OBJECTIVE:To study the impact of haifengteng on gene expression of β-APP in the cells of human neuroblastoma. DESIGN:Experimental control: medication intervention(haifengteng) and non-med ication intervention.Gene comparison between objective gene(β-APP) and structu re gene(β-Actin). MATERIALS:Cellular serials of human neuroblastoma(SK-N-SH), haifengteng. METHODS:To observe the impact of haifengteng in different reactive strength an d different reactive time on β-APP mRNA through cellular culture and RT-PCR. RESULTS:Haifengteng could selectively inhibit the gene expression of β-APP a nd the inhibition enhanced along with the prolongation of the reactive time and the increase of the reactive strength. CONCLUSION:The selective inhibition of haifengteng in gene expression of β-A PP provides a more reliable laboratorial basis in AD prevention and treatment.
出处 《中国临床康复》 CSCD 2004年第13期2592-2593,共2页 Chinese Journal of Clinical Rehabilitation
基金 国家自然科学基金(3027164) 国家中医药管理局课题(97Z301)~~
  • 相关文献

参考文献2

二级参考文献9

  • 1[1]Bitan G, Kirkitadze MD, Lomakin A, Vollers SS, Bene dek GB, Teplow DB. Amyloid beta-protein(Abeta) assembly: Abeta 40 and Abeta 42 oligomerize through distinct pathways. Proc Natl Acad Sci U S A 2003; 100 (1): 330 -5
  • 2[2]Antzutkin ON, Leapman RD, Balbach JJ, Tycko R. Supramoiecular structural constraints on Alzheimer' s beta-amyloid fibrils from electron microscopy and solid-state nuclear magnetic resonance. Biochemistry 2002; 41 (51): 15436- 50
  • 3[3]Kobayashi T, Ota S, Tanaka K, et al. A novel L266V mutation of the tau gene causes frontotemporal dementia with a unique tau pathology. Ann Neurol 2003; 53(1 ):133 - 7
  • 4[4]Cook DG, Leverenz JB, McMillan PJ, et al. Reduced hippocampal insulin-degrading enzyme in late-onset Alzheimer' s disease is associated with the apolipoprotein E-epsilon4 allele. Am J Pathol 2003; 162 (1): 313 - 9
  • 5[5]Davidsson P, Sjogren M, Andreasen N, et al. Studies of the pathophysiological mechanisms in frontotemporal dementia by proteome snalysis of CSF proteins. Brain Res Mol Brain Res 2002; 109(1 -2): 128 -33
  • 6[6]Matsuoka Y, Saito M, LaFrancois J. Novel therapeutic approsch for the treatment of Alzheimer' s disease by peripheral administration of agents with an affinity to beta-amyloid. J Neurosci2003; 23 (1): 29 - 33
  • 7[7]Weiner HL, Selkoe DJ. Inflammation and therapeutic vaccination in CNS diseases. Nature 2002; 420(6917): 879 - 84
  • 8[8]Kotwal GJ, Lahiri DK, Hicks R. Potential intervention by vaccinia virus complement control protein of the signals contributing to the progression of central nervous system injury to Alzheimer' s disease. Ann N Y Acad Sci 2002; 973:317 - 22
  • 9范文辉,李露斯,刘之荣.血管性痴呆的动物模型、神经病理及其胆碱能机制[J].中国临床康复,2002,6(21):3172-3173. 被引量:46

共引文献39

同被引文献52

引证文献5

二级引证文献54

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