Fig. 5.

Activation of STAT3 is required for ER stress-mediated inflammation in TR-iBRB cells. (a) TR-iBRB cells were treated with TM (50 ng/ml) or TG (10 nmol/l) for 8 h, and levels of phosporylated STAT3 (p-STAT3; black bars) and total STAT3 (t-STAT3; white bars) were determined by western blot analysis and quantified by densitometry (mean±SD, n=3). (b–d) TR-iBRB cells were pretreated with cucurbitacin I (Cu I) for 1 h, followed by treatment with 10 nmol/l TG for 8 h. Levels of ICAM-1, TNF-α and VEGF were determined by western blot analysis and quantified by densitometry (mean±SD, n=3). **p<0.01 vs control; ^†p<0.05, ^††p<0.01 vs TG group. (e–h) STAT3 was knocked down using siRNA (Stat3i), followed by treatment with 10 nmol/l TG for 8 h. Ctrli: scrambled/control siRNA. Knockdown efficiency was assessed from the protein level of STAT3 in cells transfected with Stat3i or transfectant only (e). Levels of ICAM-1, TNF-α and VEGF were determined by western blot analysis and quantified by densitometry (f–h, mean±SD, n=3). **p<0.01 vs Ctrli; ^††p<0.01 vs Ctrli+TG