Fig. 2: FAK inhibition suppresses LPS-induced MAPK phosphorylation.

A, B RAW 264.7 cells (RAW) were transfected with siRNA against FAK and then exposed to 0.5 μg/mL LPS for 30 min. Control cells were transfected with negative control siRNA (NC). Panel A shows immunoblots of p-FAK and FAK. Total FAK and GAPDH were used as controls. Quantification of p-FAK and FAK levels is shown in panel B [Mean ± SEM, 3 independent experiments; **P < 0.01 compared to Ctrl siRNA; ^##P < 0.01 compared to Ctrl siRNA+LPS]. C, D Activation of the MAPK pathway was assessed by measuring phosphorylated ERK, p38, and JNK in panel C. Total ERK, p38, and JNK were used as control. Quantification of p-ERK, p-JNK and p-P38 levels is shown in panel D [Mean ± SEM, 3 independent experiments; **P < 0.01 and ***P < 0.001 compared to Ctrl siRNA; ^#P < 0.05 and ^##P < 0.01 compared to Ctrl siRNA+LPS]. E–H Macrophages were pretreated with PND-1186 for 1 h prior to LPS exposure. Figure showing RAW line (E) and mouse peritoneal macrophages (MPMs; G). Concentration of PND-1186 and LPS are as indicated. Activation of the MAPK pathway was assessed by immunoblotting for phospho-proteins. Densitometric quantification of p-ERK, p-JNK and p-P38 were detected in RAW cells (F) and MPMs (H) [Mean ± SEM, 3 independent experiments; *P < 0.05, **P < 0.01 and ***P < 0.001 compared to Ctrl; ^#P < 0.05 and ^##P < 0.01 compared to LPS].