Study on the Mechanism of Acori Graminei Rhizoma in th Treatment of Alzheimer's Disease Based on Network Pharmacology and Molecular Docking

被引:3
作者
Du, Yi Kuan [1 ]
Xiao, Yue [2 ]
Zhong, Shao Min [2 ]
Huang, Yi Xing [2 ]
Chen, Qian Wen [2 ]
Zhou, Yu Qi [2 ]
Guo, Jin Yan [2 ]
Yang, Chun [2 ]
机构
[1] Southern Med Univ, Affiliated Dongguan Hosp, Cent Lab, Dongguan 523059, Guangdong, Peoples R China
[2] Guangdong Med Univ Dongguan, Key Lab Stem Cell & Regenerat Tissue Engn, Dongguan 523808, Peoples R China
关键词
TAU; CHOLINESTERASE; DERIVATIVES; INHIBITORS; PROTEIN; DESIGN; MEMORY; MICE;
D O I
10.1155/2021/5418142
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Alzheimer's disease is a common neurodegenerative disease in the elderly. This study explored the curative effect and possible mechanism of Acori graminei rhizoma on Alzheimer's disease. In this paper, 8 active components of Acori graminei rhizoma were collected by consulting literature and using the TCMSP database, and 272 targets were screened using the PubChem and Swiss Target Prediction databases. Introduce it into the software of Cytoscape 3.7.2 and establish the graph of "drug-active ingredient-ingredient target." A total of 276 AD targets were obtained from OMIM, Gene Cards, and DisGeNET databases. Import the intersection targets of drugs and diseases into STRING database for enrichment analysis, and build PPI network in the Cytoscape 3.7.2 software, whose core targets involve APP, AMPK, NOS3, etc. GO analysis and KEGG analysis showed that there were 195 GO items and 30 AD-related pathways, including Alzheimer's disease pathway, serotonin synapse, estrogen signaling pathway, dopaminergic synapse, and PI3K-Akt signaling pathway. Finally, molecular docking was carried out to verify the binding ability between Acori graminei rhizoma and core genes. Our results predict that Acori graminei rhizoma can treat AD mainly by mediating Alzheimer's signal pathway, thus reducing the production of A beta, inhibiting the hyperphosphorylation of tau protein, regulating neurotrophic factors, and regulating the activity of kinase to change the function of the receptor.
引用
收藏
页数:12
相关论文
共 41 条
[1]   BARHL1 Is Downregulated in Alzheimer's Disease and May Regulate Cognitive Functions through ESR1 and Multiple Pathways [J].
Barh, Debmalya ;
Garcia-Solano, Maria E. ;
Tiwari, Sandeep ;
Bhattacharya, Antaripa ;
Jain, Neha ;
Torres-Moreno, Daniel ;
Ferri, Belen ;
Silva, Artur ;
Azevedo, Vasco ;
Ghosh, Preetam ;
Blum, Kenneth ;
Conesa-Zamora, Pablo ;
Perry, George .
GENES, 2017, 8 (10)
[2]  
Chunxia Z., 2014, NEW DRUGS TRADITIONA, V25, P18
[3]   Inhibitory effects of eugenol on RANKL-induced osteoclast formation via attenuation of NF-κB and MAPK pathways [J].
Deepak, Vishwa ;
Kasonga, Abe ;
Kruger, Marlena C. ;
Coetzee, Magdalena .
CONNECTIVE TISSUE RESEARCH, 2015, 56 (03) :195-203
[4]   β-asarone improves learning and memory and reduces Acetyl Cholinesterase and Beta-amyloid 42 levels in APP/PS1 transgenic mice by regulating Beclin-1-dependent autophagy [J].
Deng, Minzhen ;
Huang, Liping ;
Ning, Baile ;
Wang, Nanbu ;
Zhang, Qinxin ;
Zhu, Caixia ;
Fang, Yongqi .
BRAIN RESEARCH, 2016, 1652 :188-194
[5]   Design, synthesis and evaluation of quinolinone derivatives containing dithiocarbamate moiety as multifunctional AChE inhibitors for the treatment of Alzheimer?s disease [J].
Fu, Jie ;
Bao, Fengqi ;
Gu, Min ;
Liu, Jing ;
Zhang, Zhipeng ;
Din, Jiaoli ;
Xi, Sai-Sai ;
Ding, Jinsong .
JOURNAL OF ENZYME INHIBITION AND MEDICINAL CHEMISTRY, 2020, 35 (01) :118-128
[6]  
Gao Y, 2020, J HUNAN U CHINESE ME, V40, P1515
[7]  
Haiying D., J KUNMING MED U, V40, P7
[8]  
[韩森 Han Sen], 2019, [中国中医基础医学杂志, Chinese Journal of Basic Medicine in Traditional Chinese Medicine], V25, P127
[9]   Decreased estrogen receptor-α expression in hippocampal neurons in relation to hyperphosphorylated tau in Alzheimer patients [J].
Hu, XY ;
Qin, S ;
Lu, YP ;
Ravid, R ;
Swaab, DF ;
Zhou, HN .
ACTA NEUROPATHOLOGICA, 2003, 106 (03) :213-220
[10]   Amyloid-β and tau - a toxic pas de deux in Alzheimer's disease [J].
Ittner, Lars M. ;
Goetz, Juergen .
NATURE REVIEWS NEUROSCIENCE, 2011, 12 (02) :67-72