An Analysis of the Anti-Neuropathic Effects of Qi She Pill Based on Network Pharmacology

Yong-Jia Song; Jia-Min Bao; Long-Yun Zhou; Gan Li; Kim Sia Sng; Yong-Jun Wang; Qi Shi; Xue-Jun Cui

doi:10.1155/2020/7193832

An Analysis of the Anti-Neuropathic Effects of Qi She Pill Based on Network Pharmacology

Evid Based Complement Alternat Med. 2020 May 4:2020:7193832. doi: 10.1155/2020/7193832. eCollection 2020.

Authors

Yong-Jia Song^{1

2}, Jia-Min Bao^{1

2

3}, Long-Yun Zhou^{1

2

3}, Gan Li^{1

2}, Kim Sia Sng^{1

2}, Yong-Jun Wang^{1

2

4}, Qi Shi^{1

2}, Xue-Jun Cui^{1

2}

Affiliations

¹ Spine Disease Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.
² Key Laboratory of Theory and Therapy of Muscles and Bones, Ministry of Education, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.
³ Rehabilitation Medicine College, Shanghai University of Traditional Chinese Medicine, Shanghai 200000, China.
⁴ Shanghai University of Traditional Chinese Medicine, Shanghai 200000, China.

Abstract

Background: Qi She Pill (QSP) is a traditional prescription for the treatment of neuropathic pain (NP) that is widely used in China. However, no network pharmacology studies of QSP in the treatment of NP have been conducted to date.

Objective: To verify the potential pharmacological effects of QSP on NP, its components were analyzed via target docking and network analysis, and network pharmacology methods were used to study the interactions of its components.

Materials and methods: Information on pharmaceutically active compounds in QSP and gene information related to NP were obtained from public databases, and a compound-target network and protein-protein interaction network were constructed to study the mechanism of action of QSP in the treatment of NP. The mechanism of action of QSP in the treatment of NP was analyzed via Gene Ontology (GO) biological process annotation and Kyoto Gene and Genomics Encyclopedia (KEGG) pathway enrichment, and the drug-like component-target-pathway network was constructed.

Results: The compound-target network contained 60 compounds and 444 corresponding targets. The key active compounds included quercetin and beta-sitosterol. Key targets included PTGS2 and PTGS1. The protein-protein interaction network of the active ingredients of QSP in the treatment of NP featured 48 proteins, including DRD2, CHRM, β2-adrenergic receptor, HTR2A, and calcitonin gene-related peptide. In total, 53 GO entries, including 35 biological process items, 7 molecular function items, and 11 cell related items, were identified. In addition, eight relevant (KEGG) pathways were identified, including calcium, neuroactive ligand-receptor interaction, and cAMP signaling pathways.

Conclusion: Network pharmacology can help clarify the role and mechanism of QSP in the treatment of NP and provide a foundation for further research.