Propofol suppresses adipose-derived stem cell progression via PI3K/AKT-Wnt signaling pathway.

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

Abstract (original English)

Adipose-derived stem cell (ADSC) transplantation has become a prospective way to treat cardiovascular diseases and skin traumas. Propofol, a short-acting intravenous anesthetic agent, plays an important role in the induction and maintenance of general anesthesia. In this study, we investigated the effects of propofol on ADSCs. The flow cytometry results showed that ADSCs were positive for CD29, CD44, and CD90 and negative for CD31, CD34, and CD45. The results of MTT and BrdU assays demonstrated that propofol impeded the proliferation of ADSCs. The cell scratch test showed that propofol had an inhibitory effect on the migration of ADSCs. Transwell assay showed that invasive ASDC counts decreased significantly after propofol treatment. Propofol also promoted ADSC apoptosis and arrested ADSCs in the G0/G1 phase. All these effects showed in a dose-dependent manner that the higher the concentration, the stronger the effect. Western blot analysis revealed decreased levels of FAK, PI3K, AKT, and GSK3β phosphorylation, while the phosphorylation of β-catenin increased after 48 h of treatment with propofol. The findings above indicated that the PI3K/AKT-Wnt pathways mediated propofol-inhibited ADSC proliferation, providing new insights into the propofol application in ADSCs.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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