OBJECTIVETo investigate the protective effects of adiponectin on myocardial ischemia-reperfusion injury and the potential mechanisms in rats.

METHODSThirty-two male rats aged 8 weeks were randomly assigned to sham operation (sham), myocardial ischemia-reperfusion (MIR), diltiazem treatment (diltiazem) or adiponectin administration (APN) groups (n = 8 each). MIR rats underwent left anterior descending artery (LAD) occlusion for 30 min followed by 60 min reperfusion. Diltiazem (7 microg/g) and APN (120 ng/g) were given by caudal intravenous injection at the end of 30 min ischemia and the beginning of reperfusion for rats in diltiazem or APN groups. Animals were sacrificed after 60 min reperfusion for determining the myocardial nitric oxide (NO), Caspase 3, activity of AMP-activated protein kinase(AMPK) and concentration of peroxisome proliferators-activated receptor gamma (PPARgamma). Apoptotic cells were stained by Caspase 3 Activity Assay Kit and mitochondria in myocardial cells were observed by transmission electron microscope (TEM).

RESULTSThe myocardial Caspase 3 level was significantly increased [(168.50 +/- 30.08) micromol/L vs. (53.25 +/- 11.41) micromol/L, P < 0.01], AMPK activity, PPARgamma and NO concentrations were significantly reduced in MIR group compared with those in sham group (all P < 0.05) [(0.74 +/- 0.59) IU/ml vs. (25.63 +/- 4.61) IU/ml, P < 0.01; 0.1894 vs. 0.7949, P < 0.01; (6.359 +/- 1.355) micromol/L vs. (10.396 +/- 1.901) micromol/L, P < 0.01], these effects could be significantly reversed by APN. In comparison with MIR group, the levels of Caspase 3 in cardiac muscles were significantly lowered in Adiponectin group [(88.75 +/- 6.92) micromol/L vs. (168.50 +/- 30.08) micromol/L, P < 0.01], whereas the level of AMPK and PPARgamma, NO concentration in the cardiac muscle was remarkably increased [(27.22 +/- 4.76) IU/ml vs. (0.74 +/- 0.59) IU/ml, P < 0.01; 0.8613 vs. 0.1894, P < 0.01; (15.755 +/- 1.045) micromol/L vs. (6.359 +/- 1.355) micromol/L, P < 0.01]. APN also preserved the function and structure of mitochondria in rats post ischemia/reperfusion injury. The protective pharmacologic actions of APN were superior to that of diltiazem.

CONCLUSIONAdiponectin could protect myocardial tissues from myocardial ischemia-reperfusion injury in rats, possibly by upregulating myocardial AMPK and PPARgamma expressions and preventing myocardial cells from apoptosis.