心脏衰老是指随着年龄的增长，心脏结构和心肌细胞发生形态和功能改变，并易患各种心脏疾病。心脏衰老是心力衰竭的主要诱因之一。如何预防或减缓心肌细胞衰老是未来心血管领域研究的热点。骨髓间充质干细胞（BMSCs) 通过保护缺血心肌和再生血管而改善受损心脏的功能。在前期研究，我们发现BMSCs对心肌细胞衰老具有保护作用，并且对所作用的心肌细胞具有抗氧化作用。端粒酶/端粒及SIRT1/p53信号通路在衰老发生过程中具有重要作用。据此，我们提出如下科研假设：BMSCs通过抗氧化作用（降低ROS）增加了端粒酶的活性，延长了端粒；激活心肌细胞的SIRT1，SIRT1去乙酰化p53，进而抑制下游衰老靶基因的表达，发挥抗衰老作用。本项目拟从离体和在体水平证明BMSCs的抗心肌衰老作用，并揭示其抗衰老分子信号通路，为临床上BMSCs移植应用于机体衰老的防治提供理论依据和实验支持。

Cardiac senescence is associated with significant alterations in cardiac structure and function with age and is one of the main causes of heart failure. How to prevent myocardial senescence has attracted increasing attention in cardiovascular research field. Bone marrow mesenchymal stem cells (BMSCs) improve the impaired cardiac function by protecting the ischemic myocardium and revascularization. In our previous study, we found that BMSCs produce a preventive effect on the premature senescence of neonatal rat cardiomyocytes and generate antioxidative effects in the cardiomyocytes. Telomerase/telomere and SIRT1/p53 signaling pathways play critical roles in senescence. Accordingly, we hypothesize: BMSCs exert the potent anti-aging effects on rat cardiomyocytes by antioxidative effects (decreasing ROS generation) which increase telomerase activity and telomere length and/or activate SIRT1 which deacetylates p53 and represses its activity, thereby inhibiting the expression of downstream aging genes. This study is aimed to investigate if BMSCs have anti-aging actions and reveal its anti-aging molecular signaling pathway, which will provide experimental evidence and theoretical support for BMSCs application in prevention and treatment of aging-associated diseases.