Figure 4.
The TLR4–TRIF signaling promotes hepatocyte apoptosis in fat-accumulated hepatocytes. Primary hepatocytes were isolated from wild-type (WT), TRIF-/-, and TLR4-/- mice. Cells were treated with 200 μmol/L palmitate for 24 hours to create fat-accumulated hepatocytes. Then, cells were treated with 100 ng/mL LPS for an additional 24 hours. (A) Representative pictures of terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining and (B) quantifications. Original magnification, ×400. (C) Concentrations of LDH released to supernatants were measured. Similar results were obtained in 2 independent experiments. A representative result is shown. White square, wild-type mice; black square, TRIF-/- mice; gray square, TLR4-/- mice. **P < .01. CONT, control; HPF, high-power field; PA, palmitic acids. Red horizontal bars represent average.