Effect of adipose-derived mesenchymal stem cell transplantation on inflammatory response and ventricular remodeling after myocardial infarction

ABSTRACT

BACKGROUND:

Whether adipose-derived mesenchymal stem cells are able to exert immunomodulatory effects in the treatment of myocardial infarction, as wel as the best time, is less reported.

Enzyme digestion method was employed to isolate and culture rat adipose-derived mesenchymal stem cells. By ligation of the left anterior descending coronary artery, we established animal models of myocardial infarction in 40 rats. The rats were randomly divided into four groupssham group, control group (injected high-glucose Dulbecco’s modified Eagle’s medium), 3-hour transplantation group (transplanted adipose-derived mesenchymal stem cells after 3 hours of myocardial infarction), 7-day transplantation group (transplanted adipose-derived mesenchymal stem cells after 7 days of myocardial infarction). After 14 days of operation, the levels of tumor necrosis factor-αand interleukin-10 in the plasma were detected by enzyme linked immunosorbent assay. After 28 days of operation, the left ventricular end diastolic diameter, left ventricular end systolic diameter, left ventricular ejection fraction and left ventricular fractional shortening were measured by echocardiography. RESULTS AND

Compared with the control group, in the 3-hour transplantation group and 7-day transplantation group, the levels of tumor necrosis factor-αwere significantly lower (P<0.01), and the levels of interleukin-10 were significantly higher (P<0.01) at postoperative 14 days;the left ventricular end diastolic diameter and left ventricular end systolic diameter in the two transplantation groups were also significantly smal er (P<0.05), but left ventricular ejection fraction and left ventricular fractional shortening were significantly elevated (P<0.05), which was more apparent in the 3-hour transplantation group than the 7-day transplantation group. Adipose-derived mesenchymal stem cells transplantation in acute phase of myocardial infarction can suppress the inflammatory response, regulate the cytokine network equilibrium, and thus delay ventricular remodeling and improve cardiac function.