ArticlePharmaceutical biology2026
Article in Pharmaceutical biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextBMSC senescence is associated with osteoporosis progression. Polygonatum sibiricum polysaccharide (PSP) shows potential anti-senescence activity, but its effects on bone marrow mesenchymal stem cells (BMSCs) remain unclear.
objectiveTo investigate the protective effects and molecular mechanisms of PSP against tert-butyl hydroperoxide (TBH)-induced senescence in BMSCs. MATERIALS AND
methodsSenescence was induced in primary rat BMSCs with TBH, followed by PSP intervention. Viability was assessed using the Cell Counting Kit-8 assay, while senescence-associated β-galactosidase, alkaline phosphatase, and Oil Red O staining assessed senescence and osteogenic/adipogenic differentiation. Ferritinophagy-associated proteins (NCOA4, FTH1, and LC3) and intracellular Fe
resultsPSP concentration-dependently attenuated TBH-induced senescence phenotypes in BMSCs, partially restored osteogenic differentiation, and reduced adipogenic differentiation. PSP downregulated NCOA4 expression, attenuating ferritinophagy-associated changes and intracellular Fe DISCUSSION AND
conclusionsPSP may attenuate BMSC senescence by suppressing NCOA4-mediated ferritinophagy, thereby preserving mitochondrial homeostasis and inhibiting cGAS-STING signaling. These findings provide a rationale for further investigation of PSP as a potential therapeutic strategy for osteoporosis-associated BMSC dysfunction.
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