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. 2017 Mar 27;38(7):998–1008. doi: 10.1038/aps.2016.175

Figure 7.

Figure 7

AMPK activation is essential for AS-IV alleviation of FFA-induced ER stress in hepatocytes. HepG2 cells and primary murine hepatocytes exposed to FFAs (1 mmol/L) were treated with or without AS-IV (100 μg/mL) for 24 h. Compound C (20 μmol/L) was added 1 h prior to the co-treatment with AS-IV and FFAs. Cells were treated with AICAR (1 mmol/L) for 2 h as a positive control. (A) Representative immunoblots for GRP78, CHOP, Thr981p-PERK and PERK in HepG2 cells. β-Actin was used as an internal control. (B) Densitometric analyses of the band intensity ratios for GRP78/β-actin, CHOP/β-actin and Thr981p-PERK/PERK in HepG2 cells. (C) Representative immunoblots for GRP78, CHOP, Thr981p-PERK and PERK in primary murine hepatocytes. β-Actin was used as an internal control. (D) Densitometric analyses of the band intensity ratios for GRP78/β-actin, CHOP/β-actin and Thr981p-PERK/PERK in primary murine hepatocytes. Data are presented as the mean±SEM from three independent experiments (n=3). *P<0.05, **P<0.01 compared with the control group. #P<0.05, ##P<0.01 compared with the FFA group. &P<0.05, &&P<0.01 compared with the AS-IV group. FFAs, free fatty acids; AS-IV, astragaloside IV.