ArticleJournal of dental sciences2025
Propofol-induced osteogenic differentiation in dental pulp stem cells: Modulation of MAPK signaling under inflammatory conditions.
Article in Journal of dental sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- Comparative Molecular Effects of Dexmedetomidine and Propofol on Osteoblast Migration and Osteogenic Gene Expression at Pediatric-Equivalent Concentrations: An In Vitro Study.Current issues in molecular biology · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/purpose: Bone regeneration in an inflammatory environment remains a significant challenge in the field of regenerative dentistry. Previous studies have demonstrated that inflammation inhibits osteogenic differentiation, necessitating the development of novel therapeutic approaches to counteract these effects. We investigated the effects of propofol on the osteogenic differentiation of dental pulp stem cells (DPSCs) under inflammatory conditions and explored the underlying signaling mechanisms. Materials and methods: DPSCs were cultured in the presence of lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-α) to mimic inflammatory conditions. Propofol (10, 50, and 100 μM) was administered, and its effects on cell viability, alkaline phosphatase (ALP) activity, and mineralization were assessed. In addition, the expression of osteogenic markers was analyzed and activation of the mitogen-activated protein kinase (MAPK) signaling pathway was examined by western blotting. Results: Propofol significantly enhanced ALP activity and mineralization in DPSCs under inflammatory conditions. In addition, it upregulated the expression of osteogenic marker genes and proteins. Functionally, propofol treatment activated p38 phosphorylation and suppressed extracellular signal regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) phosphorylation. Conclusion: Propofol promotes the osteogenic differentiation of DPSCs under inflammatory conditions by activating the p38/MAPK signaling while modulating the ERK and JNK pathways. This suggests that propofol has potential therapeutic applications in bone regeneration and regenerative dentistry, particularly in inflammatory environments.
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