Objective   To study the effect of simvastatin on ventricular remodeling and FoxO3a expression in rats with myocardial infarction (MI).    Methods   After a MI model of rats was established

24 survived rats were randomly divided into MI group (n=8)

simvastatin treatment group (n=8) and sham-operation group (n=10). After 4 weeks

left ventricular weight index (LVWI) and collagen volume fraction (CVF) were detected in non-infarction zone (NIZ) with Picric-Sirius red staining. mRNA and protein expression of FoxO3a in NIZ was detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Myocardial histopathology was examined with HE staining. Data were analyzed with the SAS 9.1 statistical software.    Results   The LVWI

types I and III CVF

and their ratio in NIZ were significantly higher in MI group than in sham operation (2.62±0.16 vs 1.80±0.13

18.81±2.65 vs 5.01±0.84

3.83±0.38 vs 1.52±0.23

and 4.96±0.90 vs 3.31±0.40

P0.05). The mRNA and protein expression level of FoxO3a in NIZ was significantly lower in MI group than in sham operation (0.29±0.05 vs 0.57±0.06

0.28±0.04 vs 0.62±0.07

P0.05). The LVWI

types Ⅰ and Ⅲ CVF

and their ratio in NIZ were significantly lower in simvastatin treatment group than in MI group (2.27±0.08 vs 2.62±0.16，9.26±1.13 vs 18.81±2.65

2.37±0.23 vs 3.83±0.38

and 3.98±0.79 vs 4.96±0.90，P0.05)

which were higher than those in sham operation group (P0.05). The mRNA and protein expression level of FoxO3a in NIZ was significantly higher in simvastatin treatment group than in MI group (0.49±0.06 vs 0.29±0.05

0.38±0.08 vs 0.28±0.04

P0.05)

which was lower than that in sham operation (P0.05). The improvement in lesions of myocardial tissue was better in simvastatin treatment group than in MI group (P0.05).    Conclusion   Simvastatin can effectively improve the ventricular remodeling in rats with MI. The mechanism of simvastatin may be related with its role in up-regulation of FoxO3a expression at gene transcription and protein translation level.