Objective      To determine the effect of adenovirus-angiotensin converting enzyme 2（Ad-ACE2）on the ventricular remodeling after myocardial infarction （MI） in rats.       Methods      A total of 75 Sprague-Dawley（SD） rats

at an age

of 8 to 10 weeks

weighing 200 to 250 g were randomly divided into MI model group (n=60) and sham operation group (n=15). MI model was induced by the ligation of the anterior descending branch of left coronary artery. Then the MI rats were randomly treated with normal saline

vector

and Ad-ACE2

with 15 rats in each group. The left 15 MI rats served as model control. The rats from above treatment groups were injected intramyocardial directly into normal saline

Ad-EGFP and Ad-ACE2 in 5 different points along the infarct borders respectively. Rats in the model group and sham operation group received no such injection. The relative ventricular remodeling indexes after 4 weeks were evaluated.       Results      Compared with sham operation group

ACE2 protein was highly expressed in Ad-ACE2 group（

P

0.05）. The changes of muscle fiber disorder

myofilament fracture

nuclear condensation

and nuclear fragmentation

and the elevated expression levels of type Ⅰand Ⅲcollagens in the model control were improved significantly

and decreased in Ad-ACE2 group. Immunohistochemical staining and ELISA indicated the expression levels of AngⅡ and Ang-(1-7) were increased in MI

normal saline group

vector and Ad-ACE2 groups than in the sham operation group （

P

0.05）

and that of AngⅡwas decreased

while that of Ang-(1-7) protein was increased in Ad-ACE2 group than in MI group（

P

0.05）. Western blotting showed that Ad-ACE2 injection resulted in an obvious decrease in the MMP-9 expression

a significant increase in the TIMP-1 expression

and a following reduce in the ratio of MMP-9/TIMP-1 when compared with MI control（

P

0.05）. Compared with sham operation group

the protein levels of TGF-β and α-SMA were consistently increased in MI group

normal saline group and vector group

and decreased in Ad-ACE2 group（

P

0.05）.       Conclusion      The over-expression of ACE2 ameliorates ventricular fibrosis and attenuates ventricular remodeling after MI

which probably through regulating renin-angiotensin system

down-regulating MMP-9

TGF-β

and α-SMA

and maintaining the balance of MMP-9/TIMP-1.