Psoralidin Induced Differentiation from Adipose-derived Stem Cells to Nucleus Pulposus-like Cells by TGF-β/Smad Signaling.

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)

Background Psoralidin (PL) could affect the differentiation of bone marrow mesenchymal stem cells (BMSCs). The role of PL is still unclear in adipose-derived stem cells (ADSCs). Aims This study aimed to investigate the effects of PL on ADSCs differentiation into nucleus pulposus-like cells and the TGF-β/Smad signaling pathway. Methods The proliferation and apoptosis of ADSCs were detected. The nucleus pulposus cell-related markers (CD24, BASP1, KRT19, and Aggrecan) and TGF-β/Smad signaling pathway indexes were analyzed. Results The results showed that compared to the control group, the cell activity was increased in the PL group, and the apoptosis rate was decreased. The mRNA and protein levels of nucleus pulposus cells markers (CD24, BASP1, KRT19, Aggrecan, and Collagen Type II) and TGF-β/Smad signaling pathway-related indexes (TGF-β, SMAD2, and SMAD3) were increased in PL group. After treatment with PL and TGF-β silencing, the TGF-β/Smad signaling pathway-related indicators (TGF-β, SMAD2, and SMAD3) and nucleus pulposus cells markers (CD24, BASP1, KRT19, Aggrecan, and Collagen Type II) were found to be higher in the sh-TGF-β +PL group than in the sh-TGF-β group. Conclusion In conclusion, our study showed that PL might induce the differentiation of ADSCs to nucleus pulposus cells through the TGF-β/Smad signaling pathway. It might have the potential application value in the tre

Evidence level

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

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