Abstract:
AIM To explore the effects of polydatin (PD) preconditioning on myocardial ischemia/reperfusion (I/R) injury.
METHODS Myocardial I/R injury was produced in mice via 30 min of left descending coronary artery occlusion, followed by 24 h reperfusion. Male C57/BL6J mice were randomly divided into five groups (n=18): Sham group, I/R group, I/R+PD group, I/R+PD+LY294002 group and I/R+LY294002 group. Echocardiography was employed to evaluate the cardiac functions. The area of myocardial infarction was determined by TTC staining and the levels of plasma CK and LDH were measured by ELISA. The fibrosis degree was detected by Masson staining, cardiac apoptosis was evaluated by the Tunnel assay and the expressions of p-Akt and Akt were determined by Western blot.
RESULTS Compared with those in sham group, the cardiac functions were decreased significantly (P<0.05), with enhanced CVF and apoptosis index (P<0.05) and increased levels of plasma CK and LDH (P<0.05), as well as enhanced infarct size, and the expressions of p-Akt were increased (P<0.05) in I/R group. Compared with those in I/R group, the cardiac functions were improved significantly (P<0.05), with decreased CVF and apoptosis index (P<0.05) and decreased levels of plasma CK and LDH (P<0.05), as well as decreased infarct size, and the expressions of p-Akt were further increased (P<0.05) in I/R+PD group. Compared with those in I/R+PD group, the cardiac functions were decreased (P<0.05), with enhanced CVF and apoptosis index (P<0.05) and increased levels of plasma CK and LDH (P<0.05), as well as enhanced infarct size, and the level of p-Akt was decreased (P<0.05) in I/R+PD+LY294002 group.
CONCLUSION polydatin attenuates myocardial I/R injury by activating PI3K/Akt signaling.