Fig. 7. Overexpressing IGF-1 with adenovirus vector inhibits p53 nuclear translocation via strengthening AKT1–p53 interaction.

Freshly hepatocytes, isolated from normal rats and cultured in vitro, were transfected the IGF-1 adenovirus vector to overexpress IGF-1 (called AV-IGF-1) or nontarget adenovirus vector (called AV-CTR), and then treated with H₂O₂ (200 nM) for 24 h. a The co-localization of p53 (green) with AKT1 (red) in hepatocytes of four groups (AV-CTR, AV-CTR + H₂O₂, AV-IGF-1 + H₂O₂, and AV-IGF-1), shown by immunofluorescence. Scale bar: 50 μm. b The co-localization of p53 (green) with progerin (red) in hepatocytes of four groups (AV-CTR, AV-CTR + H₂O₂, AV-IGF-1 + H₂O₂, and AV-IGF-1), shown by immunofluorescence (Scale bar: 10 and 50 μm)