Effect of C_NAA_C, a new natriuretic pepetide chimera, on myocardial damage caused by ischemia/reperfusion in rats

  AIM   To study the effect of C_NAA_C, a natriuretic peptide chimera, on myocardial damage caused by ischemia/reperfusion.

  METHODS   SD rats were randomly divided into three groups: sham, ischemia/reperfusion (I/R) and I/R + C_NAA_C groups. After occlusion of the left anterior descending coronary artery (LAD) using 6-0 silk suture for 30 min, the slipknot was released and the animal received 120 min of reperfusion. Sham group underwent the same operation procedures except that the LAD was ligated. HE staining was adopted to observe the pathological changes, transmission electron microscope was employed to observe the structure of mitochondrial morphology and TUNEL kit was used to detect myocardial apoptosis. TTC staining was used to analyze the infarct size, Elisa kits were adopted to measure humoral factors and Western blotting was used to examine the expression of related proteins.

  RESULTS   Compared with the sham group, the I/R group exhibited swelling and inflammatory infiltration in cardiomyocytes. The mitochondrial fission, the expression of cytochrome C and the myocardial apoptosis percentage were increased (P<0.01). The infarct size, the LDH, CK-MB and cTnT levels in serum were also increased (P<0.01). The expressions of PI3K and phosphorylated Akt (Ser 473) were decreased (P<0.01). Compared with the I/R group, the I/R+C_NAA_C group revealed decreased inflammatory infiltration in cardiomyocytes. The mitochondrial fission was inhibited and the expression of cytochrome C and the myocardial apoptosis percentage were decreased (P<0.01). The infarct size, abnormal LDH, CK-MB and cTnT levels in serum were also decreased (P<0.01). The expressions of PI3K and phosphorylated Akt (Ser 473) were increased (P<0.01).

  CONCLUSION   C_NAA_C up-regulates PI3K/Akt signaling pathway and ameliorates myocardial damage caused by ischemia/reperfusion.