Upregulation of Bcl-2 Through Caspase-3 Inhibition Ameliorates Ischemia/Reperfusion Injury in Rat Cardiac Allografts

Erythropoietin protects myocardium against ischemia–reperfusion injury under moderate hyperglycemia

“…EPO also attenuated the rise in cleaved capase-3 protein levels and myocardial caspase-3 activity (Fig. 7), a key initiator of apoptosis signaling pathway (Grunenfelder et al, 2001;Kirsch et al, 1999;Zeuner et al, 1999) following I/R injury. EPO induced reduction in Bcl-2 down-regulation and up-regulation of capase-3 was associated with significantly reduced degree of cardiomyocyte apoptosis and infarct size following I/R injury in HG rats as well as NG rats (Figs.…”

Antiapoptosis and Mitochondrial Effect of Pioglitazone Preconditioning in the Ischemic/reperfused Heart of Rat

“…Caspases are cysteine proteinases that have been shown to be specifically involved in the initiation and execution phases of apoptosis. Caspase-3 can be detected in cardiomyocytes [18]. Preconditioning has been reported to lower the levels of proapoptotic BAX protein in the heart [19] and prevent caspase activation during I/R [20].…”

Lipocalin-2 Regulates the Inflammatory Response During Ischemia and Reperfusion of the Transplanted Heart

“…Ischemia and reperfusion (IR) are known to negatively affect allograft function early after transplantation (1)(2)(3)(4). Cardiac IR results in disruption of the biological homeostasis followed by the induction of a complex inflammatory cascade (5)(6)(7)(8). During the early inflammatory response after IR of the myocardium, neutrophil granulocytes are activated and directed against the graft (8).…”