Abstract: AIM: To explore the possible protection mechanism of fosinopril and imidapril in reversing myocardial interstitial remodeling by observing angiotensin II (AngII) and the expression rate of caspase-3 protein, type I collagen and type III collagen. METHODS: Forty male Sprague Dawley rats were randomized into two groups: 10 in normal control group and 30 in streptozotocin-induced diabetic group. Rats in the diabetic group were subdivided into diabetic control group, fosinopril-treated group and imidapril-treated group (10 rats in each group). Fosinopril was administered at a concentration of 10 mg/kg (once daily) and imidapril was administrated at a concentration of 10 mg/kg (once daily), whereas in the diabetic control group and the normal control group, the same volume of sodium chloride was administered. Nine weeks later all rats were killed by anaesthesia. Radioimmunity was used to measure the content of AngII, ABC immunohistochemical staining was used to detect the expression rate of cysteine aspartate specific proteinase (caspase)-3 protein and SP immunohistochemical staining was used to detect the level of type I and type III collagen. RESULTS: Compared with the normal controls, left ventricular index, AngII content, expression rate of caspase-3 protein and levels of type I and type III collagen all significantly increased (P<0.05). After treatment with fosinopril and imidapril, the above indexes all improved, but no significant difference was found in the treated groups. CONCLUSION: Interstitial remodeling occurs in diabetic cardiomyopathy. Without significant difference, fosinopril and imidapril improve heart function and reduce types I and III collagen expression by decreasing the content of AngII and the expression rate of caspase-3 protein.