Fig. 6

Phosphorylation of NF-κBp65 enhanced hepatocellular proliferation through the Akt/mTOR pathway in response to inflammation. a WT mice were intraperitoneally injected with TNF-α (40 μg/kg) for 6 h, and TNF-α-induced inflammation upregulated the protein expression of ARRB1, p-Akt, p-GSK-3β, m-TOR and PCNA in mouse livers, as shown by western blotting. b Representative images of p-p65 (top), p-GSK-3β (middle) and PCNA (bottom) staining in TNF-α-induced liver inflammation. c The relative PCNA protein level and PCNA index were scored (n = 6 in each group). All values are mean ± SD. P < 0.05 using Student’s t-test. d LO2, HepG2 and Hep3B cells were treated with TNF-α (40 ng/ml) for 6 h, and the expression of ARRB1 was analysed by western blotting. TNF-α induced p-p65 expression and upregulated the protein expression of p-Akt, p-GSK-3β, m-TOR and PCNA in cell lines using western blotting. e Images showing double staining of p-p65 and EdU in TNF-α (40 ng/ml)-pretreated HepG2 cells. Shown is a representative result of three experiments. f The relative PCNA protein level and EdU index were scored. All values are mean ± SD. P < 0.05 using Student’s t-test