Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

Curcumin controls the senescence of adipose-derived mesenchymal stem cells via the FoxO3/autophagy signaling pathway to enhance joint homeostasis for osteoarthritis therapy.

Zhang R., Huang L., Jin M., Kou H., Ma J., Zhang W.

Animal Study on Osteoarthritis, Cartilage Damage, Meniscus Injury, Chronic Inflammation, published in Stem Cell Res Ther (2025) — 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
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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
Stem Cell Res Ther (2025)
Country
England
Reported sample size
—
Source database
PubMed
PMID
41318595
PMCID
PMC12771826
DOI
10.1186/s13287-025-04836-y
Citations
5

Abstract (original English)

Background Osteoarthritis (OA) is a common chronic and degenerative disease, the pathophysiological features of which involve the whole joint. In recent years, adipose tissue-derived mesenchymal stem cells (ADSCs) have attracted much attention in the field of regenerative medicine. Nonetheless, with aging in vivo or exogenous stress in vitro, mesenchymal stem cells undergo cellular senescence, resulting in limited therapeutic efficacy. Curcumin is a natural polyphenolic compound that has antioxidative, anti-inflammatory and antiapoptotic properties. We aimed to investigate the function and molecular mechanisms of the effects of curcumin on ADSC senescence and to explore the therapeutic efficacy of curcumin-pretreated ADSCs in OA management. Methods Mouse primary ADSCs were identified using immunofluorescence staining and multilineage differentiation. Cell counting kit-8 (CCK-8) assays, reactive oxygen species (ROS) level measurements, β-galactosidase staining, Western blotting, immunofluorescence staining, and transmission electron microscopy (TEM) were performed to explore the function of curcumin in ADSCs. Bioinformatics analysis, chromatin immunoprecipitation (ChIP), small interfering RNA (siRNA), and real-time quantitative PCR (RT‒qPCR) were performed to evaluate whether FoxO3 directly regulates Becn1. In vivo, adult C57BL/6 male mice were subjected to destabilization of th

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
CurcuminAnimalsOsteoarthritisMesenchymal Stem CellsMiceCellular SenescenceForkhead Box Protein O3Signal TransductionAutophagyAdipose Tissue

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