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©The Author(s) 2017.
World J Gastroenterol. Oct 28, 2017; 23(40): 7253-7264
Published online Oct 28, 2017. doi: 10.3748/wjg.v23.i40.7253
Published online Oct 28, 2017. doi: 10.3748/wjg.v23.i40.7253
Figure 1 TG induced endoplasmic reticulum stress in L02 cells.
L02 cells were treated with 1 μmol/L TG for 6, 12, 24, 36 and 48 h. Expressions of p-PERK, p-eIF2α, GADD34, GRP78, sXBP1 and CHOP were assessed by western blotting. Representative blots from three independent experiments are presented. The results of densitometric analysis are presented as a fold-change compared to that at 0 h (aP < 0.05; bP < 0.01). CHOP: C/EBP homologous protein; ER: Endoplasmic reticulum; GADD34: Growth arrest and DNA damage-inducible gene34; GRP78: Glucose-regulated protein 78; p-eIF2α: Phospho-eukaryotic translation initiation factor-2α; p-PERK: Phospho-PKR-like ER kinase; sXBP1: Spliced X box-binding protein1; TG: Thapsigargin.
- Citation: Yang FW, Fu Y, Li Y, He YH, Mu MY, Liu QC, Long J, Lin SD. Prostaglandin E1 protects hepatocytes against endoplasmic reticulum stress-induced apoptosis via protein kinase A-dependent induction of glucose-regulated protein 78 expression. World J Gastroenterol 2017; 23(40): 7253-7264
- URL: https://www.wjgnet.com/1007-9327/full/v23/i40/7253.htm
- DOI: https://dx.doi.org/10.3748/wjg.v23.i40.7253