ABSTRACT
Objectives:To explore the possible mechanisms of ischemic postconditioning on alleviating myocardial ischemia-reperfusion injury, focusing on the inflammatory-thrombus related mechanisms. Methods:Rats were randomly divided into six groups (n=10 each):sham group, ischemia-reperfusion injury group, postconditioning group, SB203580 group, anisomycin+postconditioning (Ani+postconditioning) group and anisomycin (Ani) group. After establising the model of myocardial ischemia reperfusion in rats, the levels of myocardial injury markers troponin I (TnI) and creatine kinase isoenzyme (CK-MB), level of leukocyte-platelet aggregation (PLA) were detected by flow cytometry at different time points, myocardial infarction area was measured by using TTC staining and the level of phosphorylation of p38 MAPK (P-p38 MAPK) was determined by Western blot. Results:Compared with the I/R group, the levels of CK-MB, TnI, the infarct size and the expression of PLA at 60 min and 3 h reperfusion were significantly reduced in the postconditioning group and SB203580 group (P＜0.05). Compared with the postconditioning group, the levels of above parameters were significantly higher in the SB203580 group, Ani+postconditioning group and Ani group (P＜0.05). Compared with the I/R group, the expression of P-p38 MAPK in the postconditioning group, SB203580 group, Ani+postconditioning group was significantly reduced (P＜0.05), while it was significantly upregulated in the Ani group (P＜0.05). Furthermore, compared with the postconditioning group, the expression of P-p38 MAPK in the Ani+postconditioning group and Ani group was significantly upregulated (P＜0.05). SB203580 group presented the similar protection effect as the postconditioning group. Cardioprotective effects of postconditioning was partially reduced in the Ani+postconditioning group. Conclusions:Ischemia postconditioning can reduce the expression of PLA during reperfusion by inhibiting the phosphorylation of p38MAPK, thereby attenuating myocardial ischemia-reperfusion injury.