A murine model of ischemia–reperfusion: the perfusion with leptin promotes the apoptosis-related relocation of mitochondrial proteins Bax and cytochrome c

Abstract Background Leptin exerts both protective and deleterious effects on the heart; first occurs under hypoxia- or ischemia-associated damage, second is a pro-hypertrophic factor cardiomyocytes. Therefore, leptin could represent link between obesity cardiovascular diseases. The study aimed to investigate effect of leptin—the same concentration that frequently measured in induces cardiac hypertrophy—on murine hearts following an episode ischemia–reperfusion; moreover, we evaluated heart's performance, hypertrophy, activation apoptosis. Rat were perfused continuously with without 3.1 nM for one h before 1 after ischemia. Cardiac performance was evaluated, homogenates mitochondria prepared western blot analysis actin, receptor, STAT3, pSTAT3, apoptosis-related proteins Bax, Bcl-2, cytochrome c, caspase 3. Results worsened heart recovery ischemia ( p < 0.05 Control vs IR + Lep Heart Perform, Fig. 2). Although no hypertrophic response observed, induced migration Bax release c into cytosol Lep, 5), essential events intrinsic/mitochondrial Conclusions Our results indicate presence ischemic insult reduces amplifies apoptotic signaling through mitochondrial pathway.