Objective To explore the expression of Interelenkin-17 (IL-17) and Intercellular Adhesion Molecule-1 (ICAM-1) on no-reflow phenomenon in acute myocardial infarction and reperfusion in rat.
Methods Tewelve healthy male Wistar rats were randomly divided into 2 groups: sham operation group (n = 6), and injury group (n = 6), the coronary artery of injury group rats were ligated for 60 min, then opened for 15 min, to establish the acute myocardial ischemia-reperfusion model of rat. The sham operation group was only put seam through the coronary artery without ligation. The electrocardiogram was checked before ligated, ligated 15 min, 30 min, 45 min and reperfused 15 min. After reperfusion for 15 min, the thioflavine S and Evens were injected from femoral venous, then the heart and blood were obtained (keeping only left ventricular). Hearts were sliced transversely into five to seven sections. Finally, observing if no-reflow phenomenon was existed after acute myocardial ischemia-reperfusion under the ultraviolet light (365nm). The level of serum IL-17 was detected by enzyme linked immunosorbent assay method and the expression of ICAM-1 was measured by immunohistochemical method.
Results The experiment proved that no-reflow phenomenon was existed after acute myocardial ischemia- reperfusion. Compared with the sham group, the level of serum IL-17 of injury group was increased obviously[49.75pg/mL ± 14.06 pg/mL VS 151.67pg/mL ± 11.19pg/mL, P < 0.01], the expression of ICAM-1 of myocardium in no-reflow area in injury group rats was increased obviously[64.74 ± 10.01 VS 316.16 ± 49.35, P < 0.01 ], but the expression of ICAM-1 of myocardium in no ligation region in injury group rats was no statistical significance. The level of ICAM-1 was related with the level of surm IL-17.
Conclusions The IL-17 and ICAM-1 play an imporant role in no-reflow injury. IL-17 can reduce the expession of ICAM-1 that can increases the inflammation and disfunction of the endothelial cell, then promote the no-reflow.