Investigating Alternative Treatments for Dyslipidemia Using Bioactive Compounds Derived from Kiwifruit (Actinidia chinensis): A Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulation Analysis.

INTRODUCTION

Kiwi has many bioactive compounds that may improve blood lipid levels and help treat dyslipidemia, but its molecular mechanism is not fully understood. This study explores these mechanisms using pharmacological network analysis.

METHODS

Bioactive compounds of kiwi were obtained from the IMPPAT website, and molecular targets were identified using Swiss Target Prediction and PharmMapper. Genes associated with dyslipidemia were searched in the DISGENET database. Subsequently, an enrichment analysis was conducted, and a protein-protein interaction network was constructed. Hub genes were identified. Subsequently, a molecular docking analysis was performed, followed by a molecular dynamics simulation.

RESULTS

Six bioactive compounds in kiwifruit showed good oral bioavailability and drug-likeness. Thirty-five genes linked to dyslipidemia and kiwi's targets were identified. Enrichment analysis highlighted the PPAR signaling pathway, lipid metabolism, and atherosclerosis. Hub genes included ALB, PPARG, AKT1, MMP9, PPARA, HMGCR, GSK3B, NOS3, PPARD, ACE, JAK2, and DPP4, with their interactions verified by molecular docking. Interactions between JAK2, ACE, and bioactive compounds (quinic acid and citric acid) involved spontaneous binding. Molecular dynamics simulations assessed conformational stability, mobility, solvation, and compaction of top-scoring protein-compound complexes.

DISCUSSION: Bioactive compounds in kiwifruit can modulate dyslipidemia via PPAR pathways, JAK2, and ACE, supported by docking analyses and simulations. They show therapeutic potential, pending experimental validation.

CONCLUSION

Our findings suggest how kiwi affects dyslipidemia. In silico analysis is a first step in exploring food compounds like kiwi as potential alternative treatments.