Objective：To investigate the protective effect and possible mechanism of geniposide on myocardial injury in type 1 diabetic mice. Methods：Thirty-two male C57BL/6J mice were randomly divided into 4 groups：control group，type 1 diabetes group（STZ group），geniposide 25 mg/kg administration group（GE25 group），geniposide 50 mg/kg administration group（GE50 group）. The blood glucose and body weight levels of the mice were measured. HE and Masson staining were used to detect myocardial fibrosis，immunohistochemistry was used to detect the protein expression levels of LC3B，P62，CollagenⅠand Collagen Ⅲ. H9C2 cells were cultured in vitro and divided into 4 groups：negative control group（NC），high glucose group（HG），HG + geniposide group（HG+GE），and HG+GE+ Compound C group（HG+GE+CC）. Western blot was conducted to detect the protein expression levels of autophagy-related proteins LC3BⅡ/Ⅰ，P62，Beclin1，p-AMPK，AMPK，mTOR and p-mTOR and the protein expression levels of apoptosis-related proteins BAX，BCL2，Caspase3 and Cleaved-caspase3. Results：Compared with the STZ group，the geniposide treated groups（GE25 group and GE50 group）can significantly reduce blood glucose（P < 0.01），increase the body weight（P < 0.01），reduce abnormal myocardial structure and collagen deposition（P < 0.01）in mice. Immunohistochemistry and Western blot showed that the protein expression levels of LC3BⅡ/Ⅰ，Beclin1 and p-AMPK/AMPK decreased，and the protein expression levels of CollagenⅠ，Collagen Ⅲ，P62，p-mTOR/mTOR，BAX/BCL2 and Cleaved-caspase 3/Caspase 3 increased in the STZ group. The administration of geniposide 25 mg/kg or 50 mg/kg reversed these changes. In cell experiments，geniposide pretreatment activated AMPK（increased p-AMPK/AMPK ratio）and autophagy activity（increased LC3BⅡ/Ⅰ，decreased expression of P62），and this effect was blocked by AMPK inhibitor Compound C. Conclusion：Geniposide can improve myocardial injury and reduce myocardial fibrosis in type 1 diabetic mice. The mechanism may be related to the activation of AMPK-mediated autophagy.