Objective    To investigate the mechanism by which rosiglitazone affects no-reflow following reperfusion after acute myocardial infarction (AMI).     Methods    Forty-five SD rats were randomly divided into sham-operated group

normal saline treated group and rosiglitazone treated group (at dose of 3 mg·kg

-1

·d

-1

for 14 d)

15 rats in each group. To establish no-reflow model

the rats of the latter two groups received coronary artery ligation for 3 h and reopening for 2 h. Then pathological sta

ining for no-reflow area

chemical assay for MPO activity

immunohistochemistry and RT-PCR for protein and mRNA expressions of ICAM-1 and P-selectin in myocardium were performed.     Results    No-reflow area in rosiglitazone treated group was significantly reduced

compared with that in normal saline treated group (P0.01). The MPO activity

protein and mRNA expressions of ICAM-1 and P-selectin in normal saline treated group were significantly increased (P0.01)

compared with that in sham-operated group

whereas those were significantly inhibited (P0.05) in rosiglitazone treated group.     Conclusion    Rosiglitazone can effectively reduce no-reflow area following reperfusion after AMI in rats

probably through downregulating ICAM-1 and P-selectin expressions in the myocardium after reperfusion and thereby further inhibiting adhesion and accumulation of neutrophil.