Objective   To investigate the effects of rosiglitazone

one of the PPAR-γ agonist

on angiogenesis and eNOS expression after experimental myocardial infarction (MI) in rats.    Methods   Totally 60 healthy adult SD rats were randomly and equally divided int

o 5 groups

sham operation group

control group

rosiglitazone group

rosiglitazone plus L-NAME (inhibitor of NOS) group and L-NAME group. Left anterior descending coronary was undergone permanent occlusion to establish the MI model. Rosiglitazone (3 mg·kg

-1

·d

-1

) was administered via oral gavage

and L-NAME was given by intraperitoneal injection. In 2 weeks after the corresponding treatment

the rats were sacrificed and the heart was removed. The number of microvessels positive to CD31 in the ischemic area near the infarction myocardium was counted. Western blot analysis and RT-PCR was carried out for the expressions of phosphorylized endothelial nitric oxide synthase at Ser

1177

(p-eNOS Ser

1177

) and eNOS mRNA.    Results   ①Compared with the control group

the number of CD31 positive microvessels was significantly larger in rosiglitazone group (P0.05)

but L-NAME aborted the angiogenic effect of rosiglitazone. ② The expression of eNOS mRNA in rosiglitazone group was not improved significantly compared with that in control group (P0.05)

whereas levels of p-eNOSS

1177

protein were significantly increased by rosiglitazone (P0.05).    Conclusion   Rosiglitazone can improve myocardial angiogenesis after AMI. The angiogenic effect of rosiglitazone is associated with increased phosphorylation of eNOS

and finally increases release of endothelium-derived nitric oxide (EDNO) after AMI in rats.