Decreased myocardial ischemia/reperfusion injury in ischemic preconditioning may in part involve cardiac adiponectin signal sufficiency

AIM To delineate the role of adiponectin (APN) signal pathway in ischemic preconditioning (IPC) and the underlying mechanisms. METHODSWe induced IPC and myocardial ischemia/reperfusion (MI/R) model with eight C57BL/6J mice in each group by the classical method. APN content was determined by ELISA, cardiac function was determined by noninvasive echocardiography and MI size was determined by Evans blue/TTC double staining method. Myocardial apoptosis was determined within the entire I/R region via TUNEL staining and caspase-3 activity assay and adiponectin receptor (AdipoR)/AMPK expression was determined by Western blot. RESULTSCompared with control group, APN level (19.08±2.15) μg/ml in plasma, MI/R and IPC group APN level in plasma declined (P<0.01). Compared with IPC group, APN level (15.4±2.09) μg/ml, MI/R group APN level (13.95±1.75) μg/ml was markedly decreased (P<0.05). Compared with control group, left ventricular ejection fraction (LVEF) (76.37±7.24), MI/R and IPC group LVEF were all decreased (P<0.01). Compared with IPC group LVEF (66.37±6.09), MI/R group LVEF (57.15±7.32) was markedly decreased (P<0.01). Compared with control group, left ventricular fraction shortening (LVFS) (52.13±4.80), MI/R and IPC group LVFS were all decreased (P<0.05). Compared with IPC group, LVFS (44.9±6.52), MI/R group LVFS (37±8.14) was markedly decreased (P<0.01). Compared with control group, left ventricular internal diameters of diastole (LVIDd) (3.13±0.59) mm, MI/R and IPC group LVIDd were all increased (P<0.05). Compared with IPC group LVIDd (3.23±0.50 mm), MI/R group LVIDd (3.50±0.48) mm was markedly increased (P<0.01). Compared with control group, left ventricular internal diameters of diastole (LVIDds) (1.95±0.59) mm, MI/R and IPC group LVIDds were all increased (P<0.05). Compared with IPC group LVIDds (2.15±0.21) mm, MI/R group LVIDd (2.26±0.48) mm was markedly increased (P<0.05). Compared with control group, myocardial infarct size, MI/R and IPC group myocardial infarct size were all increased (P<0.01). Compared with IPC group, myocardial infarct size (40.9±4.1), MI/R group myocardial infarct size (45.7±3.92) was markedly increased (P<0.05). Compared with control group TUNEL staining, MI/R and IPC group TUNEL staining were all increased (P<0.01). Compared with IPC group TUNEL staining (8.96 ± 1.49), MI/R group TUNEL staining (12.16±1.93) was markedly increased (P<0.05) Compared with control group, caspase-3 activity (1.93±1.82) nmol/(h·mg), MI/R and IPC group caspase-3 activity were all increased (P<0.01). Compared with IPC group caspase-3 activity (4.68±2.31) nmol/(h·mg), MI/R group caspase-3 activity (5.82±2.72) nmol/(h·mg) was markedly increased (P<0.05). Compared with control group, AdipoR1 expression (0.86±0.26), MI/R and IPC group AdipoR1 expression were all decreased (P<0.01). Compared with IPC group, AdipoR1 expression (0.72±0.22), MI/R group AdipoR1 expression (0.57±0.15) was markedly decreased (P<0.05). However, AdipoR2 expression showed no significant change. Compared with control group, pAMPK/AMPK expression (1.6±0.24), pAMPK/AMPK expression were all decreased (P<0.05). Compared with IPC group, pAMPK/AMPK expression (1.28±0.13), MI/R group AdipoR1 expression (1.04±0.13) was markedly decreased (P<0.05). CONCLUSIONDecreased myocardial ischemia/reperfusion injury in IPC may involve cardiac adiponectin signal sufficiency in part and presents the best opportunity to improve outcomes for patients after acute coronary syndrome by increasing the cardiac adiponectin signal.