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.
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
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.
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