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. 2014 Jul 28;211(8):1673–1687. doi: 10.1084/jem.20132011

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© 2014 Endo et al.

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Figure 8. — 18-HEPE administration elicited cardioprotection in TAC-operated mice. (A) %FS of post-TAC mice administered with NS, 5 µg EPA, 1 µg or 5 µg 18-HEPE i.p. every 3 d. n = 12–20. (B) Azan staining and (C) immunohistochemistry for Mac2 in ventricle sections of the mice administered with 18-HEPE after TAC. Bars, 100 µm. (D) Relative expression levels of Nppa, Col1a1, Tgfb1, and Emr1 mRNA in hearts from mice administered with 18-HEPE 4 wk after TAC. Expression levels were normalized to those of 18S ribosomal RNA, and then normalized with respect to those in the sham-operated hearts. n = 7. (E) Myocardial CSA in ventricle section of pressure-overloaded heart from the mice administered with NS, 5 µg EPA or 5 µg 18-HEPE. n = 5; n = 450–500. (F and G) 18-HEPE administration at 1 wk after TAC induction could prevent cardiac remodeling. (F) %FS of the mice administered with 18-HEPE at 5 µg every 2 d from 1 wk after TAC. n = 16 (G) Azan staining and immunohistochemistry for Mac2 in ventricle sections from the mice administered with 18-HEPE from 1 wk after TAC induction. Bars, 100 µm. n.s. indicates not significant; *, P < 0.05; **, P < 0.01 vs. N/S control group. Data in A, B, D, and F were analyzed by Kruskal-Wallis tests followed by Bonferroni post-hoc analysis. Experiments were repeated three times and the data pooled.