Hydroxyl safflower yellow A regulates bone-fat balance in osteoporosis by SphK1/S1P/S1PR signaling pathway.
Xu X., Hu X., Zhou S., Liu J., Su Z., Zheng Z.
Animal Study, published in Biochem Pharmacol (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
- Animal Study
- Journal
- Biochem Pharmacol (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40846082
- DOI
- 10.1016/j.bcp.2025.117258
Abstract (original English)
Osteoporosis is hallmarked by marrow adiposity, whereas the involvement of sphingosine kinase-1(SphK1)/sphingosine 1-phosphate (S1P)/sphingosine 1-phosphate receptors(S1PR) mediated signaling in adipocyte/osteoblast lineage commitment remains elusive. While Hydroxysafflor yellow A (HSYA) attenuates estrogen deficiency-induced bone loss, its pharmacological mechanisms remain incompletely elucidated. Our investigations in ovariectomized (OVX) murine models revealed that SphK1 ablation diminished osteoblast-specific markers (Procollagen type I N-terminal propeptide [PINP], Osteocalcin [OCN], Osteoprotegerin [OPG]), disrupted trabecular microarchitecture, and exacerbated adipose conversion through suppression of SphK1/S1PR2 coupled with Peroxisome proliferator-activated receptor gamma (PPARγ) upregulation. Pharmacological HSYA administration normalized serum estradiol and S1P concentrations, reactivated SphK1/S1P/S1PR2 axis activity, and stimulated osteogenic differentiation (Runt-related transcription factor 2 [RUNX2], Bone Morphogenetic Protein 2 [BMP2]) while concurrently inhibiting adipogenic pathways (PPARγ, CCAAT/Enhancer Binding Protein Alpha [C/EBP-α], Fatty Acid Binding Protein 4[FABP4]), leading to enhanced bone structural integrity. SphK1-deficient OVX mice displayed hypoesrogenemia, diminished bone trabecular volumetric density, and increased marrow adipocyte infiltrati
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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