全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

通络醒脑泡腾片抗痴呆的尿液代谢组学研究

Keywords: 通络醒脑泡腾片,代谢组学,Aβ25-35,阿尔茨海默症

Full-Text   Cite this paper   Add to My Lib

Abstract:

通络醒脑泡腾片(TLXNET)是源自古方芎归汤加减而来的专利处方,具有改善认知功能的作用,然而关于它对Aβ25-35海马注射痴呆模型大鼠的尿液代谢产物影响及抗痴呆作用并不明确。该实验以Aβ25-35海马注射痴呆大鼠模型为研究对象,采用代谢组学技术研究空白大鼠、Aβ25-35海马注射痴呆模型大鼠和通络醒脑泡腾片干预大鼠尿液中代谢物组时量的轨迹变化和对应关系,确定其特征性代谢标志物,并基于此标志物的代谢轨迹变化阐明通络醒脑泡腾片的抗痴呆作用。实验结果初步确定了吲哚-5,6-醌、4-羟基苯基丙酮酸(4-HPPA)、皮质醇和3-硫代乳酸等4个特征性代谢标志物,它们主要参与体内多巴胺神经系统、糖皮质激素及能量代谢途径,且通络醒脑泡腾片对4个内源性生物标记物代谢轨迹的扰动具有明显的回调作用。该实验表明Aβ25-35海马注射痴呆大鼠模型有明确的尿液代谢特征性内源性生物标志物,通络醒脑泡腾片可以通过回调其代谢轨迹的扰动而达到抗痴呆的作用。

References

[1]  L Millucci, L Ghezzi, G Bernardini,et al. Conformations and biological activities of amyloid beta peptide 25-35[J]. Curr Protein Pept Sci, 2010,11(1):54.
[2]  Limón I D, Díaz A, Mendieta L,et al. Amyloid-beta(25-35) impairs memory and increases NO in the temporal cortex of rats[J]. Neurosci Res, 2009,63(2):129.
[3]  Stepanichev M Y,MoiseevaY V.Studies of the effects of fragment (25-35) of beta am-yloid peptide on the behavior of rats in a radial maze[J]. Neurosci Behav Physiol,1998,28(5):564.
[4]  Stepanichev M Y, Moiseeva Y V, Lazareva N A,et al.Single intracerebroventricular administration of amyloid-beta (25-35) peptide induces impairment in short-term rather than long-term memory in rats[J].Brain Res Bull,2003,61(2):197.
[5]  徐世军,代渊,张荫杰,等.通络醒脑泡腾片对 Aβ海马注射痴呆大鼠 tau 蛋白磷酸化关键调控蛋白 CDK5 和 GSK-3 表达的影响[J].华西药学杂志,2013,28(2):140.
[6]  张荫杰,代渊,胡勇,等.通络醒脑泡腾片对AD大鼠学习记忆和海马胰岛素降解酶表达的影响[J].中国中药杂志, 2013,38(37):2863.
[7]  Pluskal T, Castillo S, Villar-Briones A,et al.MZmine 2: modular framework for processing, visualizing, and analyzing mass spectrometry-based molecular profile data[J].BMC Bioinformatics,2010,11:395.
[8]  李锦霞,张蔓,孙立博,等.当归挥发油给药大鼠尿液比较代谢组学研究[J].中国中药杂志,2014,39(7):1293.
[9]  Atkinsons A J, Colburn W A, DeGruttola V G, et al. Biomarkers and surrogate endpoints: preferred definitions and conceptual framework. Biomarker definition working group[J]. Clin Pharmacol, 2001, 69: 89.
[10]  Schneider P, Hampel H, Buerger K. Biological marker candidates of Alzheimer\'s disease in blood, plasma, and serum[J]. CNS Neurosci Ther, 2009, 15(4): 358.
[11]  Segura-Aguilar J, Paris I, Mu?oz P,et al.Protective and toxic roles of dopamine in Parkinson\'s disease[J].J Neurochem,2014,129(6):898.
[12]  Munoz-Munoz J L, García-Molina F, Varón R, et al.Generation of hydrogen peroxide in the melanin biosynthesis pathway[J].Biochim Biophys Acta,2009,1794(7):1017.
[13]  Barili Paolo, De Carolis Gionni, Zaccheo Damiano, et al. Sensitivity to ageing of limbic dopaminergic system: a review[J]. Mech Ageing Dev,1998,106 (1/2): 57.
[14]  Kemppainen N, Ruottinen H, Nagren K, et al. PETshows that striatal dopamine D1 and D2 receptors are differently affected in AD[J]. Neurology, 2000,55 (2): 205.
[15]  Davis K L, Davis B M, Greenwald B S,et al.Cortisol and Alzheimer\'s disease, I: basal studies[J].Am J Psychiatry,1986,143(3):300.
[16]  Csernansky J G, Dong H, Fagan A M,et al.Plasma cortisol and progression of dementia in subjects with Alzheimer-type dementia[J].Am J Psychiatry,2006,163(12):2164.
[17]  Huang C W, Lui C C, Chang W N, et al.Elevated basal cortisol level predicts lower hippocampal volume and cognitive decline in Alzheimer\'s disease[J].J Clin Neurosci,2009,16(10):1283.
[18]  Laughlin G A, Barrett-Connor E.Sexual dimorphism in the influence of advanced aging on adrenal hormone levels: the Rancho Bernardo Study[J].J Clin Endocrinol Metab, 2000,85(10):3561.
[19]  Doecke J D, Laws S M, Faux N G,et al.Blood-based protein biomarkers for diagnosis of Alzheimer disease[J].Arch Neurol,2012,69(10):1318.
[20]  Cerqueira J J, Mailliet F, Almeida O F, et al. The prefrontal cortex as a key target of the maladaptive response to stress[J]. J Neurosci,2007,27(11):2781.
[21]  Green K N, Billings L M, Roozendaal B, et al. Glucocorticoids increase amyloid-Band tau pathology in a mouse model of Alzheimer\'s disease[J]. J Neurosci,2006,26(35):9047.
[22]  Sotiropoulos I, Catania C, Riedemann T, et al. Glucocorticoids trigger Alzheimer disease-like pathobiochemistry in rat neuronal cells expressing human tau[J]. J Neurochem,2008,107(2):385.
[23]  Workman J L, Chan M Y, Galea L A.Prior high corticosterone exposure reduces activation of immature neurons in the ventral hippocampus in response to spatial and nonspatial memory[J].Hippocampus,2015,25(3):329.
[24]  Jamieson P M,Nyirenda M J,Walker B R,et al. Interactions between oestradiol and glucocortieoid regulatary effects on liver-specific glucocortieoid-inducible genes, possible evidence for a roal ofhepatic betahydroxysteroid dehydrogenase type[J]. J Endocrinol, 1999,l60: 103.
[25]  Lee S, Xu G, Jay T R,et al.Opposing effects of membrane-anchored CX3CL1 on amyloid and tau pathologies via the p38 MAPK pathway[J].J Neurosci,2014,34(37):12538.
[26]  Sanjay W, Pimplikar. Reassessing the amyloid cascade hypothesis of Alzheimer\'s disease[J]. Int J Biochem Cell Biol,2009,41(6): 1261.
[27]  Ruzzin J,Wagman A S,Jensen J. Glucocorticoid-induced insulin resistance in skeletal muscles:defects in insulin signalling and the effects of a selective glycogen synthase kinase-3 inhibitor[J]. Diabetologia,2005,48(10):2119.
[28]  German J P, Wisse B L, Thaler J P, et al. Leptin deficiency causes insulin resistance induced by uncontrolled diabetes[J]. Diabetes,2010,59(7):1626.
[29]  Costa,Mara,Pensa,et al. Preparation of 3-mercaptolactic acid and S-aminoethylmercaptolactic acid[J]. Prep Biochem,1982, 12(5):417.
[30]  张均田.脑缺血葡萄糖/脑能量代谢障碍与神经退行性疾病[J].中国药理学通报,2000,16(3):241.
[31]  陈子晟,罗焕敏.阿尔茨海默病的胆碱能药物治疗[J].中国新药杂志,2001,10(6):415.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133