What question did this study set out to answer?

This study aims to explore the mechanisms of Tian-Wang-Bu-Xin-Dan in treating Alzheimer's disease using network pharmacology.

June 10, 2026Open Access

Molecular mechanism of Tian-Wang-Bu-Xin-Dan in the treatment of Alzheimer’s disease: A network pharmacology and molecular docking study

Key Points

This study aims to explore the mechanisms of Tian-Wang-Bu-Xin-Dan in treating Alzheimer's disease using network pharmacology.
Targets of Tian-Wang-Bu-Xin-Dan and Alzheimer's disease were retrieved from multiple databases.
Pathway enrichment analyses were conducted using the DAVID tool.
Molecular docking analyzed the binding affinity between core targets and active compounds.
The TWBXD-AD network included 174 bioactive compounds and 92 overlapping targets.
Core targets involved in AD regulation included INS, AKT1, IL6, and TNF, focusing on inflammation and apoptosis.
Molecular docking suggested favorable binding of certain compounds with core targets, with Tanshinone IIA indicating a potential binding propensity.

Abstract

Introduction: Alzheimer's disease (AD) is increasing in prevalence among aging populations and presents challenges in finding effective treatments. Tian-Wang-Bu-Xin-Dan (TWBXD) is a classical remedy used to treat anxiety, insomnia, dementia, and memory disorders, with neuroprotective, vasorelaxant, hypotensive, and anti-Alzheimer's effects reported in experimental studies. This study aimed to elucidate TWBXD mechanisms in AD using network pharmacology. Methods: Targets of TWBXD and AD were retrieved from multiple databases. Pathway enrichment analyses were performed using the DAVID tool. A protein-protein interaction network was established using STRING, and topological analysis identified core targets. Molecular docking was used to examine the binding affinity between core targets and active compounds. Results: The TWBXD-AD network comprised 174 bioactive compounds and 92 overlapping targets. Enrichment analysis revealed these targets were involved in AD regulation through apoptosis (neurotrophins, PI3K-Akt, and MAPK signaling pathways), inflammation (IL-17, TNF, and C-type lectin receptor signaling pathways), and neurotransmission (serotonergic synapse and calcium signaling pathways). The most significant core targets identified were INS, AKT1, IL6, IL1B, TNF, BCL2, CASP3, and BDNF, indicating TWBXD primarily targets inflammation, apoptosis, neurotrophic factors, and neuronal growth. Molecular docking yielded favorable predicted docking scores for multiple compound–target pairs. Tanshinone IIA showed relatively low predicted docking scores with several core targets, suggesting potential binding propensity in silico. Conclusions: Active compounds and targets in TWBXD may modulate AD-related pathways associated with apoptosis, inflammation, and neurotransmission. These predictions provide valuable data for further comprehensive studies on the effects, mechanisms, and safety of TWBXD in experimental and clinical settings.

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