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. 2017 Feb 7;8:14232. doi: 10.1038/ncomms14232

Figure 3. Protective actions of FPR agonist Cmpd17b against cardiomyocyte injury responses in vitro.

Figure 3

(a) Effect of small-molecule FPR agonists (both 1 μM, added on reoxygenation) on rat cardiomyocyte cTnI release subsequent to H–R; ##P<0.01 versus sham and *P<0.05 versus vehicle-treated H–R in paired cardiomyocytes from the same preparation (one-way ANOVA, Dunnett's post hoc, n=4 separate cardiomyocyte preparations). (b) Effect of small-molecule FPR agonists (both 1 μM, added on simulated reperfusion) on mouse cardiomyocyte cTnI release subsequent to simulated I–R; ####P<0.0001 versus sham and *P<0.05 versus vehicle-treated H–R in paired cardiomyocytes from the same preparation (one-way ANOVA, Dunnett's post hoc, n=5 separate cardiomyocyte preparations). (c) Concentration-dependent Inline graphic responses to small-molecule FPR agonists Cmpd 17b (n=4) and Cmpd43 (n=5) in primary rat cardiomyocytes; *P<0.05 versus lowest concentration studied (two-way repeated measures ANOVA, Tukey's post hoc). Effect of Cmpd17b and Cmpd43 (both 10 μM) on TGF-β stimulation of cardiofibroblast. (d) Pro-fibrotic CTGF and (e) pro-inflammatory IL-1β expression; #P<0.05, ##P<0.01 versus sham and *P<0.05 versus TGF-β stimulation in paired cardiofibroblasts from the same preparation, on one-way ANOVA with Dunnett's post hoc test (n per group indicated below the x axis). Results expressed as mean±s.e.m. Controls (open symbols/bars); H–R or TGF-β (black symbols/bars); Cmpd17b (blue symbols/bars); Cmpd43 (red symbols/bars).