目的：探究Sprouty2蛋白对糖尿病心肌病纤维化程度的影响。方法：选取24只雄性SD大鼠随机分为正常组、DCM组、DCM + Sprouty2慢病毒干扰组，每组8只。DCM组、DCM + Sprouty2慢病毒干扰组高糖高脂饮食喂养4周后，腹腔注射链脲佐菌素30 mg/kg，而正常组普通饲料喂养，腹腔注射柠檬酸钠缓冲液，12周时进行慢病毒转染，16周进行超声心动图检测后处死并取材。分别进行Masson染色、天狼猩红染色、免疫组织化学和TUNEL染色。结果：与正常组相比，DCM组、DCM + Sprouty2慢病毒干扰组血糖值升高，而DCM + Sprouty2慢病毒干扰组与DCM组比较，血糖进一步升高。通过超声心动图检测发现，抑制Sprouty2蛋白表达会进一步加重心功能障碍。与正常组比较，DCM组、DCM + Sprouty2慢病毒干扰组凋亡细胞数有所增加，而DCM + Sprouty2慢病毒干扰组的凋亡细胞量明显上升。通过病理学染色观察到，敲低Sprouty2蛋白导致大量心肌纤维断裂，大量炎性细胞产生，胶原纤维表达明显升高。在免疫组化和蛋白表达上，DCM组、DCM + Sprouty2慢病毒干扰组心肌组织中α-平滑肌肌动蛋白(α-SMA)表达量升高，而DCM + Sprouty2慢病毒干扰组表达更加明显。结论：抑制Sprouty2蛋白可以促进DCM的纤维化程度，同时促进心肌细胞凋亡。因此，激活Sprouty2蛋白的表达可以逆转DCM。 Object: To investigate the effect of Sprouty2 protein on the degree of fibrosis in diabetic cardiomyopathy. Methods: Twenty-four male SD rats were randomly divided into the normal group, the DCM group and the DCM + Sprouty2 lentiviral interference group, with 8 rats in each group. After 4 weeks of high-sugar and high-fat diet feeding in the DCM and DCM + Sprouty2 lentiviral interference groups, streptozotocin 30 mg/kg was intraperitoneally injected, while the normal group was fed with normal diet and intraperitoneally injected with sodium citrate buffer, lentiviral transfection was performed at 12 weeks, and echocardiography was performed at 16 weeks before sacrifice and sampling. Masson staining, Sirius red staining, immunohistochemistry and TUNEL staining were performed, respectively. Result: Compared with the normal group, the blood glucose values were increased in the DCM and DCM + Sprouty2 lentiviral interference groups, while the blood glucose was further increased in the DCM + Sprouty2 lentiviral interference group compared with the DCM group. Inhibition of Sprouty2 protein expression further aggravates cardiac dysfunction as detected by echocardiography. Compared with the normal group, the number of apoptotic cells increased in the DCM and DCM + Sprouty2 lentiviral interference groups, while the amount of apoptotic cells increased significantly in the DCM + Sprouty2 lentiviral interference group. As observed by pathological staining, knockdown of Sprouty2 protein resulted in fragmentation of a large number of myocardial fibers, production of a large number of inflammatory cells, and markedly elevated collagen fiber expression. In immunohistochemistry and protein expression, the expression of α-smooth muscle actin (α-SMA) and vimentin in myocardial tissue was increased in the DCM and DCM + Sprouty2 lentiviral interference groups, while the expression was more pronounced in the DCM + Sprouty2 lentiviral interference group. Conclusion: Inhibition of Sprouty2 protein can promote the degree of fibrosis and myocardial apoptosis in DCM. Thus, activating the expression of Sprouty2 protein could reverse DCM.