Aim To induce myocardial fibrosis by establishing type 2 diabetes mellitus rat model,and explore prevention and treatment mechanism about Apelin-13 which is one subtype of endogenous ligand of proteins related to the angiotensin Ⅱ type 1 receptor for myocardial fibrosis of diabetes mellitus rats. Methods High fat and sugar diet combined with intravenous injection of a small dose of streptozotocin （STZ） was used to build type 2 diabetes mellitus rat model.48 Wistar rats were randomly divided into four groups: control group,model group,Apelin-13 group,blocker group （SB431542 group）.Rats in different groups were given homologous intervention for 12 weeks,specimens were collected for Masson staining to observe morphological changes and interstitial collagen deposition of myocardial,and collagen volume fraction （CVF） was measured.Contents of collagen Ⅰ and Ⅲ in myocardial tissue were detected by ELISA.Expressions of transforming growth factor-β1 （TGF-β1）,TGF-β1 receptorⅠ（TβRⅠ） were measured with immunohistochemical staining.Expressions of pathway protein smad2,p-smad2,smad3 and p-smad3 were measured by Western blot. Results Compared with control group,CVF and contents of collagenⅠand Ⅲ of myocardial tissue in model group increased obviously,accompanied with the increasing of signal transduction pathway protein TGF-β1,TβRⅠ,smad2,p-smad2,smad3 and p-smad3 （P<0.01）.Compared with model group,myocardial fibrosis dicators （CVF,collagenⅠand Ⅲ） in rats who received Apelin-13 or SB431542 significantly reduced,expressions of all pathways protein in Apelin-13 group were adjusted downward significantly （P<0.01）,differences of TGF-β1,TβRⅠhad no statistically significance between SB431542 and model group （P＞0.05）,expressions of other signal protein were obviously decreased （P<0.01）. Conclusions Exogenous Apelin-13 can restrain myocardial fibrosis in diabetes mellitus rats by weakening excessive activation of TGF-β1/TβR/smads signal transduction pathway.