XXXX reduces lung reperfusion injury.

@entity32 @entity63 @entity1457 @entity95 @entity13373 @entity651 @entity14568
BACKGROUND: The inflammatory cascade has emerged as the primary mediator of reperfusion injury. Nuclear factor kappaB (NF-kappaB) is a rapid response transcription factor that activates genes responsible for the mediators of @entity32 . @entity1457 protein 70 (HSP70) has been shown to protect against @entity651 . We hypothesized that the antioxidant @entity13373 ( @entity14568 ), an inhibitor of NF-kappaB and upregulator of HSP70, would decrease @entity651 after @entity63 and reperfusion. METHODS: Using our isolated, ventilated, blood-perfused @entity95 lung model, all groups underwent lung harvest followed by 10-h storage (4 degrees C) and blood reperfusion for 30 min. Group I lungs (n = 5) served as controls. In group II lungs (n = 5), both lung and blood donors received @entity14568 (100 mg/kg) intravenously 30 min before harvest. NF-kappaB activity was evaluated with electrophoretic mobility shift assay, and Western blot was performed for HSP70. RESULTS: Group II demonstrated superior pulmonary function. Although HSP70 expression was somewhat elevated in group II lungs, NF-kappaB binding activity was not different between the groups. CONCLUSIONS: @entity14568 improves pulmonary function after @entity63 and reperfusion in an isolated @entity95 lung model. The improved function correlates with elevated HSP70 expression during initial reperfusion, independent of NF-kappaB activity.
