Open AccessAntidepressant pathways of the Chinese herb jiaweisinisan through genetic ontology analysis
Author(s) -
Jie Chen,
Yun-Ling Huang,
Ling Li,
Jie Niu,
Weiqiong Ye,
Yunnan Wang,
Can Yan,
Lili Wu
Publication year - 2020
Publication title -
journal of integrative neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.336
H-Index - 33
eISSN - 1757-448X
pISSN - 0219-6352
DOI - 10.31083/j.jin.2020.02.1246
Subject(s) - antidepressant , computational biology , depression (economics) , gene ontology , immune system , biology , pharmacogenomics , gene , neuroscience , bioinformatics , genetics , gene expression , hippocampus , economics , macroeconomics
Active compounds and corresponding targets of the traditional Chinese herb, jiaweisinisan, were obtained from systems pharmacological database and placed into ClueGO for gene ontology analysis. The targets of depression were obtained from the Online Mendelian Inheritance in Man, the Therapeutic Target Database, and the Pharmacogenomics Knowledge Base. Compound-target and target-pathway networks were constructed using Cytoscape, and then their topological parameters were analyzed. The targets of jiaweisinisan and depression were mapped to pathways, thereby constructing antidepressant pathways of jiaweisinisan . It was found that jiaweisinisan has 82 different active compounds and 306 relevant potential targets. Also, 107 unrepeatable targets related to depression were found. In all, 26 common targets were found to be the direct anti-depression targets of j iaweisinisan and 9 pathways of jiaweisinisan related to depression were divided into three modules (synaptic transmission, cell apoptosis, and immune-inflammatory). The jiaweisinisan formula was found to have synergistic antidepressant effects due to aspects of its herb composition and the active compounds therein, giving rise to potential targets and signaling pathways related to depression. Its antidepressant mechanisms were found to mainly involve the regulation of synaptic transmission, cell apoptosis, and immune-mediated inflammation.