Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

Figure 5 Changes in protein expression and nuclear translocation of nuclear factor-κB on triggering HepG2. 2.15 cells with toll like receptor 4 specific ligand, LPS. A: Protein expression of p53 and nuclear factor-κB (NF-κB) in HepG2.2.15 cells and LPS- treated HepG2.2.15 cells. β-actin was considered as control. Quantitative analysis showed that p53 and NF-κB protein expression was repressed and upregulated respectively in treated cells; B: Confocal imaging showing nuclear uptake of NF-κB p65 subunit from cytoplasm in cells where HepG2.2.15 cells are taken as control and HepG2.2.15 cells stimulated with toll like receptor 4 (TLR4) ligand, LPS. NF-κB concentration was higher in the nucleus of LPS-treated cells compared to control cells.