摘要：SummaryCardiac hypertrophy is an adaptive response to all forms of heart disease, including hypertension, myocardial infarction, and cardiomyopathy. Cyclooxygenase-2 (COX-2) overexpression results in inflammatory response, cardiac cell apoptosis, and hypertrophy in adult heart after injury. However, immune response-mediated cardiac hypertrophy and fibrosis have not been well documented in injured neonatal heart. This study showed that cardiac hypertrophy and fibrosis are significantly attenuated in celecoxib (a selective COX-2 inhibitor)-treated P8 ICR mice after cryoinjury. Molecular and cellular profiling of immune response shows that celecoxib inhibits the production of cytokines and the expression of adhesion molecular genes, increases the recruitment of M1-like macrophage at wound site, and alleviates cardiac hypertrophy and fibrosis. Furthermore, celecoxib administration improves cardiac function at 4 weeks after injury. These results demonstrate that COX-2 inhibition promotes the recruitment of M1-like macrophages during early wound healing, which may contribute to the suppression of cardiac hypertrophy and fibrosis after injury.Graphical abstractDisplay OmittedHighlights•Cryoinjury successfully induces cardiac hypertrophy and fibrosis in P8 ICR mice•COX-2 inhibition alleviates cardiac hypertrophy and fibrosis after cryoinjury•MCP-1 significantly increases in COX-2 inhibition•COX-2 inhibition improves cardiac repair in P8 ICR mice by recruiting M1-like macrophagesAnimal Physiology; Molecular Physiology; Molecular Biology
