典型文献
Potential neuroprotection by Dendrobium nobile Lindl alkaloid in Alzheimer 's disease models
文献摘要:
At present, treatments for Alzheimer's disease can temporarily relieve symptoms but cannot prevent the decline of cognitive ability and other neurodegenerative changes. Dendrobium nobile Lindl alkaloid is the main active component of Dendrobium nobile Lindl. Dendrobium nobile Lindl alkaloid has been shown to resist aging, prolong life span, and exhibit immunomodulatory effects in animals. This review summarizes the mechanisms behind the neuroprotective effects reported in Alzheimer's disease animal models. The neuroprotective effects of Dendrobium nobile Lindl alkaloid have not been studied in patients. The mechanisms by which Dendrobium nobile Lindl alkaloid has been reported to improve cognitive dysfunction in Alzheimer's disease animal models may be associated with extracellular amyloid plaque production, regulation of tau protein hyperphosphorylation, inhibition of neuroinflammation and neuronal apoptosis, activation of autophagy, and enhanced synaptic connections.
文献关键词:
中图分类号:
作者姓名:
Dai-Di Li
作者机构:
Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Lab of Ethnomedicine of Ministry of Education,Zunyi Medical University,Zunyi,Guizhou Province,China;School of Pharmacy,Shanghai University of Traditional Chinese Medicine,Shanghai,China
文献出处:
引用格式:
[1]Dai-Di Li-.Potential neuroprotection by Dendrobium nobile Lindl alkaloid in Alzheimer 's disease models)[J].中国神经再生研究(英文版),2022(05):972-977
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Potential,neuroprotection,by,Dendrobium,nobile,Lindl,alkaloid,Alzheimer,disease,models,At,present,treatments,temporarily,relieve,symptoms,but,cannot,prevent,decline,cognitive,ability,other,neurodegenerative,changes,main,active,component,has,been,shown,resist,aging,prolong,life,span,exhibit,immunomodulatory,effects,animals,This,review,summarizes,mechanisms,behind,neuroprotective,reported,have,studied,patients,which,improve,dysfunction,may,associated,extracellular,amyloid,plaque,production,regulation,tau,protein,hyperphosphorylation,inhibition,neuroinflammation,neuronal,apoptosis,activation,autophagy,enhanced,synaptic,connections
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0.553262
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