Evidence map›Paper›PMID 42268330›Full record

ArticleMolecular biology reports2026

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

Zechun Peng, Mingbin Xu, Jie Yang, Shuming He

Abstract read
In one paragraph

Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Zechun Peng *Department of Urology II, The Second Affiliated Hospital of Hainan Medical University, No. 368 Yehai Avenue, Longhua District, Haikou, 570311, Hainan Province, People's Republic of China.
Mingbin Xu *Department of Urology II, The Second Affiliated Hospital of Hainan Medical University, No. 368 Yehai Avenue, Longhua District, Haikou, 570311, Hainan Province, People's Republic of China.
Jie YangDepartment of Urology II, The Second Affiliated Hospital of Hainan Medical University, No. 368 Yehai Avenue, Longhua District, Haikou, 570311, Hainan Province, People's Republic of China.
Shuming HeMaster of Medicine, Department of Urology II, The Second Affiliated Hospital of Hainan Medical University, No. 368 Yehai Avenue, Longhua District, Haikou, 570311, Hainan Province, People's Republic of China. heshuming163@sina.com.

Funding

the Joint Program on Health Science & Technology Innovation of Hainan Province WSJK2025QN078
6 · The paper itself

Abstract

BACKGROUND AND

objectiveNephrolithiasis 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.

methodsA 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.

resultsIntegrated 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.

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

trial registrationNot applicable.

Indexed as

Kidney CalculiNF-kappa BSulfinic AcidsTumor Necrosis Factor-alphaAnimalsCalcium OxalateCell LineDisease Models, AnimalDisulfidesHumansMaleMolecular Docking SimulationNephrolithiasisNetwork PharmacologyRatsRats, Sprague-DawleyallicinCalcium OxalateDisulfidesNF-kappa BSulfinic AcidsTumor Necrosis Factor-alphaAllicinAnimal modelKidney stonesNetwork pharmacologyTNF/NF-κB pathway

Identifiers

PMID42268330
PMCPMC13253885

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.