Figure 2.

TLR4 signalling pathway activation contributes to palmitate‐induced cell death. HepG2 cells were treated with palmitate at 0, 0.2, 0.4 and 0.6 mmol/L for overnight. Cell viability was determined by LDH release measurement (A). All values are denoted as means ± SD from three or more independent experiments. *P < .05 vs untreated cells; **P < .01 vs untreated cells. B, HepG2 cells were treated with 0.4 mmol/L palmitate at the presence/absence of CLI‐059, a TLR4 inhibitor or TLR4 neutralizing antibody for overnight. Cell viability was determined by LDH release measurement. All values are denoted as means ± SD from three or more independent experiments. Bars with different characters differ significantly (P < .05). C, Primary mouse hepatocytes were treated with 0.4 mmol/L palmitate at the presence/absence of CLI‐059, a TLR4 inhibitor or TLR4 neutralizing antibody for overnight. Cell viability was determined by LDH release measurement. All values are denoted as means ± SD from three or more independent experiments. Bars with different characters differ significantly (P < .05). D‐E, HepG2 cells were transfected with either scramble siRNA or siRNA for TLR4 for overnight, followed by 0.4 mmol/L palmitate exposure. TLR4 gene expressions were determined by real‐time PCR (D), and cell viability was measured by LDH release measurement 16 hours later. All values are denoted as means ± SD from three or more independent experiments. Bars with different characters differ significantly (P < .05)