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Objective：To explore the effect of Adenovirus-ACE2（Ad-ACE2）on ventricular remodeling after myocardial infarction（MI）in rats and thepossible protective mechanisms.Methods：MI model was induced in Sprague-Dawley(SD) rats byligating the anterior descending of left coronary artery, randomly dividedinto MI group, NS group, vector group, Ad-ACE2group, and the shamgroup. NS group, vector group and Ad-ACE2group were injectedintramyocardial directly into saline, Ad-EGFP and Ad-ACE2in fiveseparate zones along the infarction borders respectively. Rats in the MIgroup and sham group received no injection. The relative ventricularremodeling indexs after4weeks were evaluated.Results：(1) ACE2was highly efficiency and stable expressed inAd-ACE2group.(2) Compared with MI group, the changes of musclefiber disordered, myofilament fracture, nuclear condensation, nuclearfragmentation and Ⅰtype and Ⅲ type collagens in Ad-ACE2groupimproved significantly.(3) Compared with sham group, the expression levels of Ang Ⅱ protein and Ang-(1-7) protein increased in MI group, NSgroup and vector group, while the former decreased and the later increasedsignificantly in Ad-ACE2group.(4) Compared with MI group, the proteinexpression levels of MMP-9and the ratio of MMP-9/TIMP-1decreasedsignificantly in Ad-ACE2group, while the expression levels of TIMP-1protein increased.(5) Compared with sham group, the expression levels ofTGF-β and α-SMA consistently increased in MI group, NS group andvector group, and decreased significantly in Ad-ACE2group.Conclusion： ACE2overexpression could improve ameliorateventricular remodeling after MI probably by regulating RAS, andinhibiting the expression of MMP-9,TGF-β,α-SMA,improving ventricularfibrosis and maintaining the balance of MMP-9/TIMP-1.
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