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©2014 Baishideng Publishing Group Inc.
World J Gastroenterol. Nov 7, 2014; 20(41): 15289-15298
Published online Nov 7, 2014. doi: 10.3748/wjg.v20.i41.15289
Published online Nov 7, 2014. doi: 10.3748/wjg.v20.i41.15289
Figure 5 Reactive oxygen species or endoplasmic reticulum stress-induced hepatocyte death is inhibited by N-acetylcysteine treatment.
A: Western blot-assisted analysis of BCL-2, BCL-xl and β-actin; B: released lactate dehydrogenase level of primary hepatocytes after H2O2 (200 μmol) or TG (1 µmol) treatment; mean ± SD, n = 4/group, bP < 0.01 vs Ctrl group; dP < 0.01 vs H2O2 group; fP < 0.01 vs Ctrl group; hP < 0.01 vs TG group; C: schematic illustration of NAC works in IR-stressed liver. NAC: N-acetylcysteine; IR: Ischemia-reperfusion; Ctrl: Control; ROS: Reactive oxygen species.
- Citation: Sun Y, Pu LY, Lu L, Wang XH, Zhang F, Rao JH. N-acetylcysteine attenuates reactive-oxygen-species-mediated endoplasmic reticulum stress during liver ischemia-reperfusion injury. World J Gastroenterol 2014; 20(41): 15289-15298
- URL: https://www.wjgnet.com/1007-9327/full/v20/i41/15289.htm
- DOI: https://dx.doi.org/10.3748/wjg.v20.i41.15289