TY - JOUR T1 - Peroxiredoxin II Inhibits Alcohol-induced Apoptosis in L02 Hepatocytes Through AKT/β-Catenin Signaling Pathway JF - Anticancer Research JO - Anticancer Res SP - 4491 LP - 4504 DO - 10.21873/anticanres.14454 VL - 40 IS - 8 AU - YING-HAO HAN AU - WEI-LONG LI AU - MEI-HUA JIN AU - YING-HUA JIN AU - YOUNG-QING ZHANG AU - LING-ZU KONG AU - LI-YUN YU AU - JIN WON HYUN AU - JEONGWOO KWON AU - HU-NAN SUN AU - TAEHO KWON Y1 - 2020/08/01 UR - http://ar.iiarjournals.org/content/40/8/4491.abstract N2 - Background: Peroxiredoxin II (PRDX2) performs unique roles in cells. It can reduce peroxides through cysteine residues, and helps prevent the effects of oxidative stress on cells. It is closely related to the occurrence and development of various diseases, especially alcoholic liver injury and even liver cancer. The metabolism of alcohol in hepatocytes leads to the increase in the levels of reactive oxygen species (ROS), oxidative stress, injury, and apoptosis. Therefore, this study focused on the investigating the protection conferred by PRDX2 against alcohol-induced apoptosis of hepatocytes. Materials and Methods: PRDX2 inhibition of alcohol-induced apoptosis in L02 hepatocytes was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, fluorescence microscopy, flow cytometry, western blotting and hematoxylin and eosin staining. Results: The results showed that the levels of reactive oxygen species, protein kinase B, β-catenin, B-cell lymphoma-2 (BCL2), BCL-XL, BCL2-associated X, cleaved caspase-3, and cleaved poly (ADP-ribose) polymerase in PRDX2-silenced cells were increased significantly after the treatment of cells with ethanol. Similar results were obtained in an in vivo Prdx2-knockout mouse model of alcoholic liver injury. Therefore, PRDX2 may regulate the phosphorylation of the AKT signal protein by eliminating reactive oxygen species from cells, and it inhibits the downstream mitochondria-dependent apoptosis pathway, and, thereby, the apoptosis of cells. Conclusion: Thus, PRDX2 may be a potential molecular target for the prevention and treatment of alcoholic liver injury. ER -