Figure 4.
17R-RvD1 prevents the activation of NF-κB–dependent pathways and reduces NLRP3 inflammasome. (A) Activated phosphorylated NF-κB p65 (p-NF-κB p65) in heart cells identified with immunofluorescence staining (size scale bar, 20 μm) in SS mice exposed to H/R stress and treated with either vehicle or 17R-RvD1 (left). Data are presented as mean ± SEM (n = 5). °P < .05 (compared with vehicle-treated H/R SS mice by t test). Quantification of total NF-κB in heart cells is shown in supplemental Figure 8B. Immunoblot analysis (right), using specific antibodies against p-NF-κB p65 and NF-κB p65, of heart 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). A total of 75 μg/μL of protein loaded on an 8% T, 2.5% C polyacrylamide gel. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) serves as protein loading control. One representative gel from 4 with similar results is shown. Densitometric analysis of immunoblots is shown (right). Data are presented as means ± SEM (n = 4). ∗P < .05 (compared with normoxia); °P < .05 (compared with vehicle-treated mice by 1-way ANOVA). (B) Immunoblot analysis, using specific antibodies against P-selectin, ET-1, and thromboxane synthase (TBXS), in the hearts of AA and SS mice treated. A total of 75 μg/μL of protein loaded on an 11% T, 2.5% C polyacrylamide gel. GAPDH serves as protein loading control. One representative gel from 4 with similar results is shown. Densitometric analysis of immunoblots is shown (right). Data are presented as means ± SEM (n = 4). ∗P < .05 (compared with normoxia); §P < .05 (compared with AA normoxia); °P < .05 (compared with vehicle-treated mice by 1-way ANOVA). (C) Immunoblot analysis, using specific antibodies against NLRP3, in the hearts of AA and SS mice, treated similar to panel B. A total of 75 μg/μL of protein loaded on an 8% T, 2.5% C polyacrylamide gel. GAPDH serves as protein loading control. One representative gel from 4 with similar results is shown. Densitometric analysis of immunoblots is shown (lower). Data are presented as means ± SEM (n = 4). ∗P < .05 (compared with normoxia); °P < .05 (compared with vehicle-treated mice). Wb, Western blot.

17R-RvD1 prevents the activation of NF-κB–dependent pathways and reduces NLRP3 inflammasome. (A) Activated phosphorylated NF-κB p65 (p-NF-κB p65) in heart cells identified with immunofluorescence staining (size scale bar, 20 μm) in SS mice exposed to H/R stress and treated with either vehicle or 17R-RvD1 (left). Data are presented as mean ± SEM (n = 5). °P < .05 (compared with vehicle-treated H/R SS mice by t test). Quantification of total NF-κB in heart cells is shown in supplemental Figure 8B. Immunoblot analysis (right), using specific antibodies against p-NF-κB p65 and NF-κB p65, of heart 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). A total of 75 μg/μL of protein loaded on an 8% T, 2.5% C polyacrylamide gel. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) serves as protein loading control. One representative gel from 4 with similar results is shown. Densitometric analysis of immunoblots is shown (right). Data are presented as means ± SEM (n = 4). ∗P < .05 (compared with normoxia); °P < .05 (compared with vehicle-treated mice by 1-way ANOVA). (B) Immunoblot analysis, using specific antibodies against P-selectin, ET-1, and thromboxane synthase (TBXS), in the hearts of AA and SS mice treated. A total of 75 μg/μL of protein loaded on an 11% T, 2.5% C polyacrylamide gel. GAPDH serves as protein loading control. One representative gel from 4 with similar results is shown. Densitometric analysis of immunoblots is shown (right). Data are presented as means ± SEM (n = 4). ∗P < .05 (compared with normoxia); §P < .05 (compared with AA normoxia); °P < .05 (compared with vehicle-treated mice by 1-way ANOVA). (C) Immunoblot analysis, using specific antibodies against NLRP3, in the hearts of AA and SS mice, treated similar to panel B. A total of 75 μg/μL of protein loaded on an 8% T, 2.5% C polyacrylamide gel. GAPDH serves as protein loading control. One representative gel from 4 with similar results is shown. Densitometric analysis of immunoblots is shown (lower). Data are presented as means ± SEM (n = 4). ∗P < .05 (compared with normoxia); °P < .05 (compared with vehicle-treated mice). Wb, Western blot.

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