Fig. 3.

ER stress upregulates inflammatory genes and mediates high-glucose-induced inflammation in TR-iBRB cells. (a–e) TR-iBRB cells were treated with TM or TG for 8h. (a) Level of GRP78 was determined by western blot analysis. (b–d) Production of ICAM-1 (b), TNF-α (c) and VEGF (d) was determined in whole cell lysate by western blot analysis and quantified by densitometry (mean±SD, n=3). (e) Protein level of VEGF secreted into the medium was determined by ELISA (mean±SD, n=5). *p<0.05, **p<0.01 vs control. (f–j) TR-iBRB cells were treated with high glucose with or without chemical chaperone PBA or TUDCA for 16 h. Production of ICAM-1 (f), TNF-α (g) and VEGF (h) was determined by western blot analysis and quantified by densitometry (mean±SD, n=3). (i) Protein level of VEGF in the medium was determined by ELISA (mean±SD, n=5). *p<0.05, **p<0.01 vs high glucose (HG). (j) Representative blots showing no difference in ICAM-1, TNF-α or VEGF levels in TR-iBRB cells treated with normal glucose with or without TUDCA or PBA for 16 h