Pharmacological Inhibition of NLRP3 Inflammasome Attenuates Myocardial Ischemia/Reperfusion Injury by Activation of RISK and Mitochondrial Pathways

Figure 1

Infarct area, LDH release, and contractility recovery in hearts from rats exposed to 30 min of ischemia plus 60 min of reperfusion, pretreated or not with 50 µM INF4E in the perfusate 20 min before ischemia. (a): infarct size after IR exposition is expressed as a percentage of ischemic tissue (% IS/IT). (b): LDH release in the perfusion effluent during the IR was expressed as units per mg of wet tissue weight. (c)–(e): monitoring of left ventricular pressure (LVP) was used to assess the contractility response to ischemia reperfusion injury. (c) shows the percentage of contractility recovered at the end of 60 min reperfusion. (d) and (e) show the entire time-course of developed LVP (DLVP) and end diastolic LVP (EDLVP), respectively. Data are means of 6 rats ± SEM. versus IR. < 0.01 versus IR.

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