中文摘要：

AIM:To investigate the effects of N-acetylcysteine(NAC) on endoplasmic reticulum(ER) stress and tissue injury during liver ischemia reperfusion injury(IRI).METHODS:Mice were injected with NAC(300 mg/kg) intraperitoneally 2 h before ischemia.Real-time polymerase chain reaction and western blotting determined ER stress molecules(GRP78,ATF4 and CHOP).To analyze the role of NAC in reactive oxygen species(ROS)-mediated ER stress and apoptosis,lactate dehydrogenase(LDH) was examined in cultured hepatocytes treated by H2O2 or thapsigargin(TG).RESULTS:NAC treatment significantly reduced the level of ROS and attenuated ROS-induced liver injury after IRI,based on glutathione,malondialdehyde,serum alanine aminotransferase levels,and histopathology.ROS-mediated ER stress was significantly inhibited in NAC-treated mice.In addition,NAC treatment significantly reduced caspase-3 activity and apoptosis after reperfusion,which correlated with the protein expression of Bcl-2 and Bcl-xl.Similarly,NAC treatment significantly inhibited LDH release from hepatocytes treated by H2O2 or TG.CONCLUSION:This study provides new evidence for the protective effects of NAC treatment on hepatocytes during IRI.Through inhibition of ROS-mediated ER stress,NAC may be critical to inhibit the ER-stressrelated apoptosis pathway.

英文摘要：

AIM: To investigate the effects of N-acetylcysteine (NAC) on endoplasmic reticulum (ER) stress and tissue injury during liver ischemia reperfusion injury (IRI).