ABSTRACT
BACKGROUND:Studies have shown that inflammatory cytokines may influence the prognosis after myocardial infarction, and play an important role in the process of cardiac remodeling. The non-hematopoietic effects of erythropoietin have been confirmed:erythropoietin can reduce the inflammatory reaction through bending with the erythropoietin on the surface of target cel membrane, thus decreasing the reperfusion injury after myocardial ischemia. OBJECTIVE:To observe the effect of recombinant human erythropoietin on the inflammatory factor expression during cardiac remodeling in rats with acute myocardial infarction. METHODS: Sprague Dawley rat models of acute myocardial infarction were established through the ligation of the left anterior descending coronary artery. The rats were divided into five groups:sham operation group was injected with normal saline;operation control group was injected with normal saline after modeling;SB203580 group was injected with highly selective p38 MAPK inhibitor SB203580 after modeling;erythropoietin group was injected with erythropoietin after modeling;the erythropoietin+SB203580 group was injected with erythropoietin+SB203580 mixed solution after modeling. The tail vein blood samples were col ected before modeling, 1 day, 1 week, 2 weeks and 4 weeks after modeling, and then enzyme-linked immunosorbent assay was used to detect the levels of interleukin-1β, interlrukin-6 and tumor necrosis factor-α. RESULTS AND CONCLUSION:There were no significant differences in the levels of interleukin-1β, interlrukin-6 and tumor necrosis factor-αbetween groups before modeling (P>0.05). There were no significant differences in the levels of interleukin-1β, interlrukin-6 and tumor necrosis factor-αbetween different time points in the sham operation group (P>0.05), and the levels were highest at 1 day after modeling in the other four groups, and then decreased at 4 weeks after modeling (Perythropoietin+SB203580 group (P0.05). Recombinant human erythropoietin can inhibit the expressions of inflammatory factors (interleukin-1β, interlrukin-6 and the tumor necrosis factor-α) during cardiac remodeling after rat acute myocardial infarction, and the mechanism of recombinant human erythropoietin for inhibiting the expressions of inflammatory factors may related with the transforming growth factorβ1-TAK1-p38 MAPK signal pathway.