Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMed

ASPP-092, a Curcuma comosa diarylheptanoid, inhibits the adipogenic differentiation of human bone marrow-derived mesenchymal stem cells via activation of TGF-β/SMAD2/3 signaling.

Sutjarit N., Yanukun K., Bhukhai K., Asavapanumas N., Rangketkarn S., Thongsa-Ad U.

Laboratory Study on Chronic Inflammation, published in Biomed Pharmacother (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
Laboratory Study
Journal
Biomed Pharmacother (2025)
Country
France
Reported sample size
—
Source database
PubMed
PMID
41365115
DOI
10.1016/j.biopha.2025.118884

Abstract (original English)

Excessive bone marrow adipose tissue (BMAT) is a key contributor to postmenopausal osteoporosis. It is associated with bone marrow-derived mesenchymal stem cells (BM-MSCs), which favor differentiation into adipocytes, thereby compromising osteoblast and bone formation. In addition, BMAT secretes anti-osteogenic factors that exacerbate bone loss. In this study, we investigated the effects of ASPP-092, a diarylheptanoid compound isolated from Curcuma comosa, on BM-MSC differentiation. ASPP-092 inhibited adipogenic differentiation and lipid accumulation by downregulating key adipogenic transcription factors and enzymes, including peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), sterol regulatory element-binding protein 1 (SREBP1), lipoprotein lipase (LPL), and fatty acid-binding protein 4 (FABP4). ASPP-092 also reduced the secretion of pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) while increasing anti-inflammatory interleukin-10 (IL-10) and adipokines such as leptin, adiponectin, and resistin. Transcriptomic analysis revealed upregulation of genes involved in the transforming growth factor-beta (TGF-β), Hippo, and Wnt/beta-catenin signaling pathways. Pharmacological inhibition of TGF-β/SMAD2/3 signaling abolished the anti-adipogenic effects of ASPP-092. These findings identify a nove

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
HumansMesenchymal Stem CellsDiarylheptanoidsCurcumaSmad2 ProteinAdipogenesisTransforming Growth Factor betaSignal TransductionSmad3 ProteinCell Differentiation

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