Selenoprotein P attenuates oxidative senescence and ferroptosis-associated lipid peroxidation in dental pulp stem cells through a FOXM1-dependent program

Figure 2 Selenoprotein P/selenite co-treatment attenuates H₂O₂-induced senescence and preserves dental pulp stem cell functional competence. A: Experimental design for the oxidative stress-induced dental pulp stem cell (DPSC) senescence model and treatment groups [blank, control, and treatment (recombinant selenoprotein P + sodium selenite)]; B: Representative SA-β-gal staining images showing senescence-associated morphological changes in DPSCs across groups. Scale bars = 50 μm; C: Quantification of SA-β-gal-positive cells; D: Western blot analysis of senescence markers (P53, P21, and P16), selenoprotein P, and the proliferation marker proliferating cell nuclear antigen; E: Densitometric quantification of the proteins shown in panel D; F: Representative EdU staining images showing DNA synthesis/proliferation in DPSCs. Scale bars = 50 μm; G: Quantification of the percentage of EdU-positive cells; H: CCK-8 assay showing growth curves/viability of DPSCs across groups; I: Western blot analysis of stemness markers (OCT4 and THY1) and the DNA damage marker γH2AX; J: Densitometric quantification of OCT4, THY1, and γH2AX. Data are presented as mean ± SD. ^aP < 0.05. DPSC: Dental pulp stem cell; SEPP1: Selenoprotein P; PCNA: Proliferating cell nuclear antigen.