Allicin inhibits kidney stone formation by suppressing the TNF/NF-κB pathway: Experimental validation through network pharmacology, in vitro, and in vivo studies

Nephrolithiasis is a prevalent urological disorder characterized by significant incidence and frequent recurrence. Allicin has diverse pharmacological effects; however, its precise function and underlying mechanisms in reducing kidney stone formation have not been thoroughly investigated. The present research endeavors to comprehensively examine the impact of allicin on the development of renal calculi and elucidate its underlying mechanisms.

A multifaceted methodology was implemented, incorporating network pharmacology for target and pathway identification, molecular docking to evaluate binding affinities, in vitro experiments utilizing calcium oxalate-damaged HK-2 cells for assessing cellular responses, and in vivo investigations employing ethylene glycol-induced nephrolithiasis rat model to examine physiological impacts.

Integrated network pharmacological screening identified 46 overlapping targets shared by allicin and nephrolithiasis. Among these hub molecules, TNF was recognized as the central effector target, and the TNF/NF‑κB signaling axis was determined as the dominant pathway mediating the protective effects of allicin against renal crystal formation. Molecular docking confirmed that allicin moderately binds to TNF (binding energy of -2.05 kcal/mol). In vitro, allicin (200 µmol/L) improved the viability of injured HK-2 cells and decreased the levels of inflammatory factors. In vivo, allicin reduced kidney damage and calcium oxalate deposition in rats.

Allicin alleviates kidney stones by inhibiting the TNF/NF-κB pathway, providing preclinical evidence for its potential in kidney stone management.

Not applicable.