A Network Pharmacology Approach to Reveal the Underlying Mechanisms of Paeonia lactiflora Pall. On the Treatment of Alzheimer's Disease

被引：29

作者：

Zeng, Qiang ^{[1
,2
,3
]}

Li, Longfei ^{[4
]}

Jin, Yu ^{[2
,3
]}

Chen, Zongzheng ^{[1
,2
,3
]}

Duan, Lihong ^{[2
,3
]}

Cao, Meiqun ^{[2
,3
]}

Ma, Min ^{[1
]}

Wu, Zhengzhi ^{[2
,3
]}

机构：

[1] Jinan Univ, Sch Tradit Chinese Med, Integrated Chinese & Western Med Postdoctoral Res, Guangzhou 510632, Guangdong, Peoples R China

[2] Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Shenzhen 518035, Guangdong, Peoples R China

[3] Shenzhen Inst Geriatr, Shenzhen 518020, Guangdong, Peoples R China

[4] Southwest Med Univ, Sch Pharm, Dept Pharmacol, Lab Mol Pharmacol, Luzhou 646000, Peoples R China

来源：

EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE | 2019年 / 2019卷

基金：

中国国家自然科学基金;

关键词：

BETULINIC ACID; MOUSE MODEL; RAT MODEL; NEUROINFLAMMATION; PROTEIN; INHIBITION; DEFICIT; TRIALS; BETA;

D O I：

10.1155/2019/8706589

中图分类号：

R [医药、卫生];

学科分类号：

10 ;

摘要：

Objective. To investigate the potential active compounds and underlying mechanisms of Paeonia lactiflora Pall. (PLP) on the treatment of Alzheimer's disease (AD) based on network pharmacology. Methods. The active components of PLP were collected from Traditional Chinese Medicine System Pharmacology (TCMSP) database, and their possible target proteins were predicted using TCMSP, SwissTargetPrediction, and STITCH databases. The putative AD-related target proteins were identified from Therapeutic Target Database (TTD), GeneCards, and MalaCards database. The compound-target-disease network interactions were established to obtain the key targets about PLP acting on AD by network topology analysis. Then, the function annotation and signaling pathways of key targets were performed by GO and KEGG enrichment analysis using DAVID tools. Finally, the binding capacity between active ingredients and key targets was validated by molecular docking using SystemsDock tools. Results. There were 7 active compounds involving in 151 predicted targets identified in PLP. Besides, a total of 160 AD-related targets were identified. Among these targets, 30 shared targets of PLP and AD were acquired. After topological analysis of the PLP potential target-AD target network, 33 key targets that were highly responsible for the therapeutic effects of PLP on AD were obtained. Further GO and KEGG enrichment analysis showed that these key targets were significantly involved in multiple biological processes and pathways which participated in cell apoptosis and inflammatory response and maintained the function of neurons to accomplish the anti-AD activity. The molecular docking analysis verified that the 7 active compounds had definite affinity with the key targets. Conclusions. The ameliorative effects of PLP on AD were predicted to be associated with regulating neural cell apoptosis, inflammatory response, and neurotrophy via various pathways such as PI3K-Akt signaling pathway, MAPK signaling pathway, and neurotrophin signaling pathway.

引用

页数：12