Fig. 7.
Effect of NF-κB inhibition on pulmonary apoptosis and injury. A: kidney IRI induced TUNEL positivity in lungs of both vehicle-treated and Bay 11-treated mice (FC = 8.84 ± 1.44 vs. 6.2 ± 1.7, AV = 1.68 ± 0.27 vs. 1.18 ± 0.33, P = 0.402), both of which were increased compared with sham. B: representative lung micrographs of TUNEL staining at 24 h exhibit increased apoptosis in both vehicle and Bay-11 groups. C: kidney IRI induced more caspase-3 positivity in Bay-11-treated groups compared with vehicle-treated groups (FC = 2.96 ± 0.64 vs. 6.13 ± 0.70†, AV = 1.63 ± 0.35 vs. 3.37 ± 0.38, P = 0.03), both of which were increased compared with sham. D: representative lung micrographs of cleaved caspase-3 immunohistochemistry show increased cleaved caspase-3-positive cells in both vehicle and Bay-11 groups after IRI. E: BAL protein was measured at 24 h in vehicle-treated and Bay-11-treated mice following sham or ischemic AKI. Similar to vehicle-treated mice (48.7 ± 1.7 vs. 75.8 ± 6.6*, P = 0.01), Bay-11-treated mice demonstrated increased BAL protein leak during kidney IRI compared with sham (21.1 ± 2.4 vs. 53.1 ± 8.4*, P = 0.006). Whereas there was no difference in BAL protein leak following IRI between vehicle-treated and Bay-11-treated mice (75.8 ± 6.6 vs. 53.1 ± 8.4, P = 0.09), Bay-11 mice had decreased BAL protein after sham compared with vehicle-treated groups (48.7 ± 1.7 vs. 21.1 ± 2.4†, P = 6.005 × 10−5). n ≥ 5/group, *P < 0.05 for IRI vs. sham, †P < 0.05 for vehicle vs. Bay-11.