AIM:To investigate the protective effect of heme oxygenase-1(HO-1)against H_(2)O_(2)-induced apoptosis in human ARPE-19 cells.METHODS:The lentiviral vector expressing HO-1 was prepared and transfected into apoptotic A...AIM:To investigate the protective effect of heme oxygenase-1(HO-1)against H_(2)O_(2)-induced apoptosis in human ARPE-19 cells.METHODS:The lentiviral vector expressing HO-1 was prepared and transfected into apoptotic ARPE-19 cells induced by H_(2)O_(2).Functional experiments including cell counting kit-8(CCK-8)assay,flow cytometry(FCM)and mitochondrial membrane potential assay were conducted.RESULTS:The ultrastructure of ARPE-19 cells was observed using transmission electron microscope(TEM).It was found that exogenous HO-1 significantly ameliorated H_(2)O_(2)-induced loss of cell viability,apoptosis and intracellular levels of reactive oxygen species(ROS)in ARPE-19 cells.The overexpression of HO-1 facilitated the transfer of nuclear factor erythroid-2-related factor 2(Nrf2)from cytoplasm to nucleus,which in turn upregualted expressions HO-1 and B-cell lymphoma-2(Bcl-2).Furthermore,HO-1 upregulation further inhibited H_(2)O_(2)-induced release of cysteinyl aspartate specific proteinase-3(caspase-3).CONCLUSION:Exogenous HO-1 protect ARPE-19 cells against H_(2)O_(2)-induced oxidative stress by regulating the expressions of Nrf2,HO-1,Bcl-2,and caspase-3.展开更多
基金Supported by Natural Science Foundation of Fujian Province(No.2017J01274)Health Science and Technology Program of Fujian Province(No.2015-ZQNJC-26)Quanzhou Science and Technology Plan Project(No.2016Z053)。
文摘AIM:To investigate the protective effect of heme oxygenase-1(HO-1)against H_(2)O_(2)-induced apoptosis in human ARPE-19 cells.METHODS:The lentiviral vector expressing HO-1 was prepared and transfected into apoptotic ARPE-19 cells induced by H_(2)O_(2).Functional experiments including cell counting kit-8(CCK-8)assay,flow cytometry(FCM)and mitochondrial membrane potential assay were conducted.RESULTS:The ultrastructure of ARPE-19 cells was observed using transmission electron microscope(TEM).It was found that exogenous HO-1 significantly ameliorated H_(2)O_(2)-induced loss of cell viability,apoptosis and intracellular levels of reactive oxygen species(ROS)in ARPE-19 cells.The overexpression of HO-1 facilitated the transfer of nuclear factor erythroid-2-related factor 2(Nrf2)from cytoplasm to nucleus,which in turn upregualted expressions HO-1 and B-cell lymphoma-2(Bcl-2).Furthermore,HO-1 upregulation further inhibited H_(2)O_(2)-induced release of cysteinyl aspartate specific proteinase-3(caspase-3).CONCLUSION:Exogenous HO-1 protect ARPE-19 cells against H_(2)O_(2)-induced oxidative stress by regulating the expressions of Nrf2,HO-1,Bcl-2,and caspase-3.
