Dapagliflozin (DAPA) exerts cardioprotective effects in non-diabetic patients. Nonetheless, the protective mechanism remains unknown. This study aims to evaluate the performance of DAPA on cardiac function and remodeling as well as its potential mechanism in mice with myocardial infarction (MI). Here, a MI mice model was established. One week after MI, mice were treated with saline or DAPA (1.5 mg/kg/day) for 4 weeks. At the end of this study, echocardiography was performed to assess cardiac structure and function. Myocardial apoptosis was analyzed by Western blot and immunofluorescence. Inflammatory cytokines and cardiac fibrosis were analyzed by real-time PCR and Masson’s trichrome stain, respectively. Results showed that DAPA improved cardiac structure and function, attenuated cardiac fibrosis, and inhibited inflammatory cytokines and myocardial apoptosis. Moreover, the inhibition of PI3K/AKT/mTOR pathway might be related to the cardioprotective role of DAPA. These findings reveal that dapagliflozin is a potential therapeutic agent for MI patients without diabetes.

达格列净 (DAPA) 对非糖尿病患者具有心脏保护作用。尽管如此，保护机制仍然未知。本研究旨在评估 DAPA 对心肌梗死 (MI) 小鼠心脏功能和重构的影响及其潜在机制。在这里，建立了 MI 小鼠模型。MI 后一周，用盐水或 DAPA（1.5 mg/kg/天）治疗小鼠 4 周。在本研究结束时，进行了超声心动图评估心脏结构和功能。通过蛋白质印迹和免疫荧光分析心肌细胞凋亡。分别通过实时 PCR 和 Masson 三色染色分析炎性细胞因子和心脏纤维化。结果表明，DAPA 改善了心脏结构和功能，减轻了心脏纤维化，并抑制炎性细胞因子和心肌细胞凋亡。此外，PI3K/AKT/mTOR通路的抑制可能与DAPA的心脏保护作用有关。这些发现表明，达格列净是非糖尿病 MI 患者的潜在治疗剂。