Figure 5. OxLDL induces TLR4-dependent activation of p38 MAPK in primary SMCs.
(A)–(C) SMCs were incubated for increasing amount of time (30, 60,120 and 240 min with 50 ug/mL)of oxLDL. The phosphorylation of p38 and NF-κB was detected by Western blotting (A) and quantified by densitometry in 3 independent experiments (B and C) as relative units (p38 or NF-κB phosphorylated protein/total protein). (Mean ± SD, n = 3; *P<0.05, **P<0.01 compared with con group). (D)- (G) The primary SMCs of TLR4−/− (C57BL/6 as control) and TLR4 antibody blocking (mouse IgG as control) have been treated with or without oxLDL (50 ug/mL) for 240 min to measure the activation of p38 or NF-κB in 3 independent experiments as relative units (p38 or NF-κB phosphorylated protein/total protein). (Mean ± SD, n = 3; **P<0.01 compared with oxLDL untreated group, ##P<0.01 compared with C57BL/6 group, $P<0.05, $$P<0.01 compared with mouse IgG group).