17R-RvD1 prevents H/R activation of acute inflammatory response pathways and reduces SCD vascular vulnerability through multimodal action on NF-κB activation. (A) BAL protein content (upper panel) and leukocyte content (lower panel) from AA and SS mice under normoxia and treated with vehicle or 17R-RvD1 (100 ng) and exposed to H/R: hypoxia (8% oxygen; 10 hours), followed by reoxygenation (21% oxygen; 3 hours) (upper panel). All data are mean ± SD (n = 6). (B) Immunoblot analysis, using specific antibodies against phosphorylated (P-)NF-κB, NF-κB, P-Nrf2, and Nrf2, in lung from AA and SS mice treated as in (A) (left panel). Vertical line(s) in NF-κB, P-p65 gel have been inserted to indicate a repositioned gel lane. One representative gel from 6 gels with similar results is presented. Densitometric analysis of immunoblots (right panels). Data are mean ± SD (n = 6 in each group). (C) Expression of miR-126 (mmu–miR-126-5p), as determined using quantitative polymerase chain reaction, in the lungs of AA and SS mice undergoing H/R and 17R-RvD1 treatment. Results are mean ± SD from 3 to 6 mice per group. (D) Immunoblot analysis, using specific antibodies against HO-1, IL-6, ET-1, ICAM-1, PDGF-B, and TXAS-1, of lung from AA and SS mice treated as in (B). One representative gel from 6 gels with similar results is shown. Densitometric analysis immunoblots are shown in supplemental Figure 2A. *P < .05 vs normoxia, °P < .05 vs healthy mice (AA), ^P < .05 vs vehicle.