N-acetylcysteine attenuates reactive-oxygen-species-mediated endoplasmic reticulum stress during liver ischemia-reperfusion injury

Figure 4 Reactive oxygen species-mediated endoplasmic reticulum stress is inhibited by N-acetylcysteine treatment in vitro. A: Endoplasmic reticulum stress related gene (GRP78, ATF4 and CHOP) expressions in primary hepatocytes harvested 3 h after H₂O₂ treatment by quantitative real-time reverse transcriptase polymerase chain reaction analysis; mean ± SD, n = 3-5/group, ^bP < 0.01, ^dP < 0.01, ^hP < 0.01 vs Ctrl group; ^aP < 0.05, ^fP < 0.01, ^gP < 0.05 vs NAC + H₂O₂ group; B: western blot-assisted analysis of GRP78, ATF4, CHOP and β-actin; C: Relative quantities of protein of GRP78, ATF4 and CHOP, mean ± SD, n = 3-5/group, ^bP < 0.01, ^dP < 0.01, ^fP < 0.01 vs Ctrl group; ^aP < 0.05, ^cP < 0.05, ^hP < 0.01 vs NAC + H₂O₂ group; representative of three experiments. NAC: N-acetylcysteine; IR: Ischemia-reperfusion; Ctrl: Control.