Abstract: Objective To study the effect of apelin-13 on myocardial fibrosis in diabetic rats and its underlying mechanism. Methods SD rats were randomly divided into control group, diabetic model group, low apelin-13 dose group and high apelin-13 dose group.Rats in control group were fed with ordinary diet and those in low and high apelin-13 dose groups were fed with high fat and sugar diet for 4 weeks.A diabetic model of rats was then established by injecting streptozotocin (STZ) at the dose of 30 mg/kg into their abdominal cavity.Eight weeks after the rats in low and high apelin-13 dose groups received intra-gastric STZ at the dose of 50 μ g/(kg · d) and 100 μ g/(kg · d) respectively, their cardiac index and left ventricular mass index (LVMI) were calculated. Morphology of collagen in myocardial tissue was observed with Masson staining, collagen volume fraction (CVF) in left ventricular interstitial tissue was measured by image analysis, local Ang Ⅱ level was measured by radioimmunoassay, and expressions of TGF-β 1 protein, MMP-1 and its inhibitor were detected by Western blot. Results The cardiac index, LVMI, CVF in left ventricular interstitial tissue, and the Ang Ⅱ level and the TGF-β 1 and TIMP-1 protein expression levels were significantly higher whereas the MMP-1 expression level was significantly lower in diabetic model group than in control group (P ＜ 0.05). These indexes significantly improved in a dosedependent manner, especially in high apelin-13 dose group. Conclusion Apelin-13 improves myocardial fibrosis in diabetic rats by down-regulating the expression of MMP-1 and TIMP-1.