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. 2008 Jun 24;5(6):e137. doi: 10.1371/journal.pmed.0050137

Figure 10. Renal Ischemia and Preconditioning in A2BAR Bone Marrow Chimeric Mice.

Figure 10

A2BAR bone marrow chimeric mice [A2BAR+/+→A2BAR+/+ [WT→WT], A2BAR−/−→A2BAR−/− [KO→KO], A2BAR−/−→A2BAR+/+ [KO→WT] and A2BAR+/+→A2BAR−/− [WT→KO]) were generated. Experiments were performed 8 wk following transplantation. Mice underwent right nephrectomy and underwent 45 min of left renal artery ischemia with or without prior IP (consisting of four cycles of 4 min ischemia followed by 4 min reperfusion). Following 24 h of reperfusion time, (A) plasma creatinine and (B) GFRs were measured.

Influence of A2BAR agonist (BAY 60–6583) on renal function in bone marrow chimeric mice exposed to ischemia. A2BAR bone marrow chimeric mice were subjected to 45 min of ischemia with or without treatment with A2BAR agonist BAY 60–6583 (60 μg/kg intravenous). Following 24 h of reperfusion, (C) plasma creatinine, (D) GFR, and (E) histological tissue injury (Jablonski index) were obtained.

Statistics: (A–D) One-way ANOVA with Tukey's post-hoc test was performed (**, p < 0.001 versus the respective group without IP. The F-test results are (A) F (7,40)= 24.82, p < 0.001; (B) F (7,40) = 48.04, p < 0.001; (C) F (3,20) = 15.54, p < 0.001; (D) F (3,20) = 20.88, p < 0.001.

(E) Kruskal-Wallis nonparametric analysis (chi-square = 12, df = 3, p = 0.007) with follow-up pairwise comparisons by Wilcoxon-Mann-Whitney test was performed with *, p < 0.05 versus WT mice with BAY treatment.