Male Wistar rats weighing 240 to 280 g were anesthetized with sodium pentobarbital and ventilated with oxygen enriched room air using DAPT Inhibitor a rodent ventilator. The left carotid artery was cannulated for monitoring arterial pressure and electrocardiogram leads were placed to record heart rate. The chest was opened by a left thoracotomy in the fifth intercostal space. After pericardiotomy, a 6 0 prolene ligature was placed under the left coronary artery where it emerges from beneath the left atrial appendage and the ends were threaded through a small plastic tube to form a snare for reversible LCA occlusion. Complete LCA occlusion was confirmed by observing cyanosis of the myocardium as well as ST segment deviation. Experimental protocol Rats were randomized into five groups, as shown in Fig ure 1 sham Inhibitors,Modulators,Libraries group the ligature was placed under the LCA without occlusion.

I/R group no interventions were applied either before or after LCA occlusion. PostC Inhibitors,Modulators,Libraries group three cycles of 10 s of reperfusion and 10 s of reocclusion immediately at the onset of reperfusion. PostC Ag490 group the JAK2 inhibitor AG 490 was administered 5 min before PostC. PostC wortmannin group the PI3K inhibitor wortmannin was administered 5 min before PostC. Other two control groups, treating rats with Ag490 or wortmannin alone without PostC, were designed to eval uate the effects of Ag490 and wortmannin alone in I/R group. The doses of AG490 and wortman nin were according to previous study. Additional rats from the sham and PostC groups were treated with 0. 1% DMSO to detect any indepen dent effects of the DMSO vehicle.

Myocardial Inhibitors,Modulators,Libraries biopsies from the sham group were obtained at 20 min, 2. 5 h or 24 h after thoracotomy. The other groups were subjected to 30 min of LCA occlu sion followed by 10 min, 2 h or 24 h of reperfusion. Myocardial biopsies were taken at the end of the experiment. The PostC protocol was per formed with three cycles of 10 s of reperfusion and 10 s of reocclusion immediately at the onset of reperfusion as reported previously. Myocardial infarction size analysis After reperfusion, the LCA was re ligated at its original site. 2 ml of 2% evans blue was injected into the inferior vena cava to define the area at risk. The ventri cles of the hearts were sliced transversely into 2 mm thick slices. The slices were incubated in 1% triphenylte trazolium chloride at 37 C for 15 min to identify the infarction size.

AAR and IS were deter mined by computerized planimetry using Inhibitors,Modulators,Libraries ImageJ soft ware. AAR was expressed as a percentage of the left ventricle and IS was expressed as a percentage of the AAR. TUNEL staining The histochemical detection of apoptotic cells was per Inhibitors,Modulators,Libraries formed as previously reported. The tissue blocks were fixed in 4% paraformaldehyde and incubated with Enzastaurin chemical structure proteinase K. Fragments of DNA in the tissue sections were analyzed using a TUNEL detection kit.