Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Diallyl Disulfide Mitigates LPS-Induced Inhibition of Osteogenic Differentiation and Alleviates Inflammatory Bone Loss via PI3K/AKT Signaling Pathway

Wu J., Guo D., Du Y., Wang Z., Li S., Xu H.

Animal Study on Chronic Inflammation, published in Drug Des Devel Ther (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Drug Des Devel Ther (2026)
Reported sample size
—
Source database
Europe PMC
PMID
42007397
PMCID
PMC13091635
DOI
10.2147/dddt.s590959

Abstract (original English)

Background Systemic inflammation impairs bone health by inhibiting the osteogenic differentiation of bone marrow stromal cells (BMSCs), thereby contributing to bone loss. Diallyl disulfide (DADS), a natural compound with anti-inflammatory properties, was investigated for its ability to mitigate inflammatory bone loss (IBL), reverse LPS-induced suppression of osteogenic differentiation, and elucidate the underlying mechanisms. Methods An LPS-induced mouse model of IBL was used to evaluate the effects of DADS by micro-CT, histological and immunohistochemical staining, and serum ELISA. An in vitro model was established by exposing BMSCs to LPS. The optimal concentration of DADS was determined using a Cell Counting Kit-8 (CCK-8) assay. Osteogenic differentiation was evaluated by alkaline phosphatase (ALP) staining, Alizarin Red S (ARS) staining, immunofluorescence, and Western blot. Network pharmacology and transcriptome sequencing were employed to identify potential therapeutic mechanisms, and the PI3K/AKT pathway was verified using the inhibitor LY294002. Results Micro-CT and histological analyses confirmed that DADS attenuated bone loss in the IBL mouse model. Toluidine blue staining and immunohistochemical analysis demonstrated that DADS promoted osteogenic differentiation. Immunohistochemical detection and serum ELISA of inflammatory cytokines revealed that DADS significantly

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Cells, CulturedMesenchymal Stem CellsAnimalsMice, Inbred C57BLMiceDisease Models, AnimalInflammationDisulfidesAllyl CompoundsLipopolysaccharides

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