In sickle cell mice, 17R-RvD1 preserves cardiac contractility and protects against H/R-induced neutrophil heart infiltration. (A) Fractional shortening (FS [%]) in SS mice under normoxia and exposed to H/R stress and treated with either vehicle or 17R-RvD1 (n = 3-4); P < .05 (compared with vehicle-treated H/R SS mice). (B) Serum Gal-3 from AA and SS mice under normoxia and treated with vehicle or 17R-RvD1. Data are presented as mean ± SEM (n = 5-9). ∗∗∗∗P < .005 (by unpaired t test with Welch correction). (C) Immunofluorescence expression of Gal-3 (red) in heart microsections from AA mice and SS mice exposed to H/R stress treated with either vehicle or 17R-RvD1. Nuclei (blue) were stained with DAPI. Quantification of Gal-3 was performed on 3 to 4 samples per group (6 × 400 field per sample) with ZEN 2.3 Software. Data are presented as mean ± SEM (n = 3-4). ∗P < .05; ∗∗∗P < .001 (by 1-way ANOVA). (D) Heart neutrophils infiltration identified, by flow cytometric analysis, as CD45⁺Ly6G⁺ cells 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). Data are presented as mean ± SEM (n = 4). ∗P < .05 (compared with normoxia); °P < .05 (compared with vehicle-treated H/R SS mice by 1-way ANOVA). (E) One representative image by immunomicroscopy (left) and quantification (right) of proresolving CD206-polarized intracardiac neutrophils (per mm² heart tissue) identified by double immunofluorescence for Ly6G and CD206 in SS mice exposed to H/R and treated with vehicle or 17R-RvD1. Data are presented as mean ± SEM (n = 3-4). °P < .05 (compared with vehicle-treated H/R SS mice by t test; size scale bar, 40 μm). MFI, mean fluorescence intensity.