Human Umbilical Cord Blood Mononuclear Cells Inhibit Rabbit Cardiac Myocyte Apoptosis After Acute Myocardial Infarction

ObjectiveTo observe the effects of human umbilical cord blood mononuclear cells on rabbit cardiac myocyte apoptosis after acute myocardial infaretion(AMI).Methods45 Chinese rabbits were divided into three groups randomly: Cells transplantation group with 15 rabbits was intravenously administrated with HUCBC labeled with bromodexyuridine(BrdU) at 24h after myocardial infarction; Control group with 15 rabbits was intravenously administrated with saline at 24h after myocardial infarction. the sham operation group with 15 rabbits, not receiving ligation of coronary artery, was intravenously administrated with saline at 24h after operation. Cardiac funtions were performed by echocardiography at 1st week, 2nd week and 4th week after transplantation. The survival of transplanted cells and the expression of Bcl-2, Bax were identified in the myocardium by immunohistochemistry. The apoptotic cells were detected in the myocardium by TUNEL.Results:(1) Compared to control group, transplantation of HUCBC improved left ventricular function indexs such as LVFS,LVEF at all 3 examinations(P<0.01); (2) Immunohistochemistry showed that only in the transplanted group, BrdU positive cells were found in the myocardial infarction area and also in the walls of vessels; (3) Compared to the control group at 4 weeks after the transplantation, the expression of Bax was decreased significantly(P<0.05), while the expression of Bcl-2 was increased significantly in the transplantation group(P<0.05),; (4) Compared to the control group at 4 weeks after the transplantation, the cardiomyocyte apoptotic index was decreased significantly in the transplantation group(P<0.05).Conclusions:(1) Intravenous administration of HUCBCs obviously improved the heart function; (2) The HUCBCs by intravenous administration could migrate into the peri-infarcted area and also survive in the peri-infarcted area. (3) The HUCBCs by intravenous transplantation could enhance the expression of Bcl-2 and inhibit the expression of Bax in the peri-infarcted area. (4) The HUCBCs by intravenous administration could inhibit cardiomyocyte apoptosis in the peri-infarcted area. The results suggested that anti-apoptosis induced by the HUCBCs might be the one of main mechanisms for stem cell transplatation for myocardial infarction.