Abstract: AIM: To examine the effect of recombinant human insulin-like growth factor-I(rhIGF-I) on the expression of matrix metalloproteinases (MMPs) and interstitial degradation of myocardium in postinfarction rats. METHODS: Seven-week old male Sprague-Dawley (SD) rats were intraperitoneally injected with isoprenaline to establish myocardial infarction (MI) model. Forty-eight rats showed clear ECG evidence of infarction and were assigned randomly to IGF-I group (rhIGF-I 50 μg·kg^-1·d^-1, i.v.), Oct group (Octreotide 50 μg·kg^-1·d^-1, i.v.) or MI group (normal sodium 5 mL·kg^-1·d^-1, i.v.). Each group was divided into two subgroups (n=8, respectively) according to the treatment days, 2 or 14 days when the rats were sacrificed. Another 8 normal SD rats were selected as the control group. Transthoracic echocardiograms were performed to examine the thickness of anterior wall (LVAW) and posterior wall (LVPW) of left ventricle, left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD), and fractional shortening (FS) as well. The levels of MMP-2, MMP-9, TIMP-1 in myocardium were quantified with immunohistochemistry. Tissue homogenate myocardium hydroxyproline concentration was determined by pepsis method.RESULTS: Compared with the MI group, the expressions of MMP-2 and MMP-9 in rhIGF-I group were decreased, and the expression of TIMP-1 in the infarcted areas was increased;the degradation of myocardium collagen were decreased and the LVEDD and LVESD were decreased, the FS was increased; the expressions of MMP-2 and MMP-9 in Oct group were increased, the degradation of myocardium collagen was aggravated, the LVAW was decreased, the LVEDD, LVESD were increased, the FS was decreased.CONCLUSION: rhIGF-I administered to rats after MI is associated with decreased activities of MMPs, substantial increase of expression of TIMP-1, and leads to attenuate interstitial degradation of myocardium and may improve ventricular remodeling.

Key words: insulin-like growth factor-I, myocardial infarction, ventricular remodeling, matrix metalloproteinase, tissue inhibitor of metalloproteinase-I