Matches in Nanopublications for { ?s ?p "NHBE cells were pretreated with 0.5 to 5 ?M BAY 11-7082 before hyperoxic exposure. BAY 11-7082 is an irreversible NF-?B inhibitor that inhibits the IKK pathway to phosphorylate I?B, which is then degraded [24] and [25]. Figure 3 shows that pretreatment of NHBE cells with BAY 11-7082 accelerated hyperoxia-induced cell death. This accelerated loss of cell viability is independent of the presence of 0.5% DMSO, the vehicle for BAY 11-7082, because the extents of cell viability upon exposure to hyperoxia were similar in cells with or without 0.5% DMSO (Fig. 3). In contrast, an increase in the dose of BAY 11-7082 resulted in an incremental loss of cell viability in hyperoxia, indicating that inhibition of NF-?B can induce an accelerated, dose-dependent cell killing effect. These data suggest a protective role for NF-?B against hyperoxia-induced nonapoptotic cell death." ?g. }
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- _3 value "NHBE cells were pretreated with 0.5 to 5 ?M BAY 11-7082 before hyperoxic exposure. BAY 11-7082 is an irreversible NF-?B inhibitor that inhibits the IKK pathway to phosphorylate I?B, which is then degraded [24] and [25]. Figure 3 shows that pretreatment of NHBE cells with BAY 11-7082 accelerated hyperoxia-induced cell death. This accelerated loss of cell viability is independent of the presence of 0.5% DMSO, the vehicle for BAY 11-7082, because the extents of cell viability upon exposure to hyperoxia were similar in cells with or without 0.5% DMSO (Fig. 3). In contrast, an increase in the dose of BAY 11-7082 resulted in an incremental loss of cell viability in hyperoxia, indicating that inhibition of NF-?B can induce an accelerated, dose-dependent cell killing effect. These data suggest a protective role for NF-?B against hyperoxia-induced nonapoptotic cell death." provenance.