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. 2012 Dec 18;168(1):238–252. doi: 10.1111/j.1476-5381.2012.02176.x

Figure 4.

Figure 4

Role of FPR subtypes in Ac-ANX-A12–26 cardioprotection in the rat isolated heart ex vivo, on the time course of protection in the presence of Ac-ANX-A12–26 (0.3 μM), alone or in the presence of the non-selective FPR-antagonist Boc2 (10 μM), the FPR1-selective antagonist CsH (1 μM), or the FPR2-selective antagonist QuinC7 (10 μM) during reperfusion. (A) Both Boc2 and CsH (both P < 0.05, n = 6) significantly inhibited Ac-ANX-A12–26–induced protection of myocardial LDH release, but QuinC7 had no effect (P = NS, n = 6). Similar attenuation of the Ac-ANX-A12–26 effect by Boc2 and CsH, but not QuinC7, was also evident on recovery of both (B) LVDP and (C) LV + dP/dt. The AUC results for Ac-ANX-A12–26 cardioprotection ± FPR antagonists are also shown, on (D) LDH release, (E) LVDP and (F) LV + dP/dt. Sham n = 9, untreated I–R, n = 15 and Ac-ANX-A12–26–treated I–R, n = 17. *P < 0.05 untreated I–R versus sham; #P < 0.05 Ac-ANX-A12–26–treated I–R versus untreated I–R rat hearts; §P < 0.05, §§P < 0.01 and §§§P < 0.001 antagonist + Ac-ANX-A12–26–treated I–R versus Ac-ANX-A12–26–treated I–R and †P < 0.05, ††P < 0.01 and †††P < 0.001 antagonist + Ac-ANX-A12–26–treated I–R versus untreated I–R rat hearts respectively.