Integrated Network Pharmacology and Proteomic Analyses of Targets and Mechanisms of Jianpi Tianjing Decoction in Treating Vascular Dementia

Jidan Liu; Juanfen Gong; Jinchao Xu; Mengyuan Fang; Meng Su; Weiguang Li; Yiyi Wu; Yang Hui; Yingchun He

doi:10.1155/2023/9021546

Integrated Network Pharmacology and Proteomic Analyses of Targets and Mechanisms of Jianpi Tianjing Decoction in Treating Vascular Dementia

Evid Based Complement Alternat Med. 2023 Jan 18:2023:9021546. doi: 10.1155/2023/9021546. eCollection 2023.

Authors

Jidan Liu¹, Juanfen Gong¹, Jinchao Xu², Mengyuan Fang¹, Meng Su¹, Weiguang Li¹, Yiyi Wu³, Yang Hui⁴, Yingchun He¹

Affiliations

¹ Department of Geriatrics, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou 310000, Zhejiang, China.
² Department of Sports Medicine, The Second Affiliated Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou 350000, Fujian, China.
³ Department of Intensive Care Unit, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou 310000, Zhejiang, China.
⁴ Department of Emergency, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou 310000, Zhejiang, China.

Abstract

Background: Vascular dementia (VD), associated with cerebrovascular injury, is characterized by severe cognitive impairment. Jianpi Tianjing Decoction (JTD) has been widely used to treat VD. However, its molecular targets and mechanisms of action in this treatment remain unclear. This study integrated network pharmacology and proteomics to identify targets and mechanisms of JTD in the treatment of VD and to provide new insights and goals for clinical treatments.

Methods: Systematic network pharmacology was used to identify active chemical compositions, potential targets, and mechanisms of JTD in VD treatment. Then, a mouse model of VD was induced via transient bilateral common carotid artery occlusion to verify the identified targets and mechanisms of JTD against VD using 4D label-free quantitative proteomics.

Results: By screening active chemical compositions and potential targets in relevant databases, 187 active chemical compositions and 416 disease-related compound targets were identified. In vivo experiments showed that JTD improved learning and memory in mice. Proteomics also identified 112 differentially expressed proteins in the model and sham groups and the JTD and model groups. Integrating the network pharmacology and proteomics results revealed that JTD may regulate expressions of cytochrome c oxidase subunit 7C, metabotropic glutamate receptor 2, Slc30a1 zinc transporter 1, and apolipoprotein A-IV in VD mice and that their mechanisms involve biological processes like oxidative phosphorylation, regulation of neuron death, glutamate secretion, cellular ion homeostasis, and lipoprotein metabolism.

Conclusions: JTD may suppress VD development via multiple components, targets, and pathways. It may thus serve as a complementary treatment option for patients with VD.