Prostaglandin E1 protects hepatocytes against endoplasmic reticulum stress-induced apoptosis via protein kinase A-dependent induction of glucose-regulated protein 78 expression

Figure 6 Prostaglandin E1 protected against endoplasmic reticulum stress-induced apoptosis via induction of glucose-regulated protein 78 expression in both L02 and HepG2 cells. L02 and HepG2 cells were transfected with either siRNA scramble control (ConsiRNA) or siRNA against human GRP78 (GRP78 siRNA) for 48 h. The cells were treated with 1 μmol/L PGE1 for 12 h and 24 h. A and B: Expressions of GRP78 in L02 cells and in HepG2 cells were detected by western blotting. One representative blot each from the three individual experiments is presented. The results of densitometric analysis are presented as a fold-change compared to those at 0 h (^bP < 0.01); C: mRNA expression of GRP78 in L02 cells was detected by real-time PCR. Histograms represent mean ± SD of three experiments (^aP < 0.05; ^bP < 0.01 vs those at 0 h). D and F: Apoptotic indices of L02 cells and HepG2 cells were determined by flow cytometry. Histograms represent mean ± SD of five independent experiments, each of which was performed in triplicate (^dP < 0.01 vs those of TG + PGE1 at the same time point; ^fP < 0.01 vs those of TG at the same time point); E and G: Cell viability of L02 cells and HepG2 cells was determined by MTS assay. Histograms represent mean ± SD of five independent experiments, each of which was performed in triplicate (^dP < 0.01 vs those of TG + PGE1 and ^fP < 0.01 vs those of TG at the same time point). GRP78: Glucose-regulated protein 78; PGE1: Prostaglandin E1; MTS: [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium]; siRNA: Small interfering RNA; TG: Thapsigargin.