目前认为，高血压病、心力衰竭以及动脉粥样硬化等均是衰老相关性心血管疾病，与心肌细胞衰老密切相关，通过调控心肌细胞衰老防治此类疾病具有重要临床意义；而端粒-端粒酶系统失稳是心肌细胞衰老的核心机制。既往研究提示中药活性成分具有防治细胞衰老的作用，附子多糖（FPS）携带还原性的半缩醛羟基，抗氧化作用明显，但是FPS是否具有延缓心肌细胞衰老的作用及机制并不明确。我们已发表的文章报道，FPS能改善大鼠高脂血症和缺血再灌注损伤。我们预实验的结果证实，FPS在人工衰老动物模型以及体外衰老心肌细胞模型中，均能有效延缓心肌衰老，同时稳定端粒-端粒酶系统。本课题拟在此基础上，以动物、细胞、分子为研究对象，探讨FPS延缓心肌衰老的作用，同时以p19ARF/p53/p21Cip1信号通路为切入点，阐述FPS通过此通路稳定端粒-端粒酶系统，延缓心肌衰老的分子机制。这将为把FPS作为心肌衰老的治疗新靶点提供理论依据。

Myocardial cell aging is the most important pathological physiology change during cardiovascular aging associated diseases. So regulating myocardial cell aging has important clinical significance. Polysaccharide from Fuzi (FPS) is a polysaccharide extracted from Fuzi. It can have redox reaction with the active oxygen for it contains hemiacetal hydroxyl. Cell aging is also closely related to oxidative stress, but whether FPS can delay cell aging and its mechanism are not clear. Our previous published articles report that FPS can improve aging associated diseases such as hyperlipidemia and atherosclerosis in rats. Our previous work find that as human aging developed, telomere length is reduced accordingly. Besides, telomere length also is reduced if the patients are suffering from aging associated chronic diseases. What’s more, FPS can improve the aging indexes in the aging Wistar rat model dose-dependently. In addition, FPS delays cell aging in the primary cardiomyocytes. The aim of this study is to detect the role of FPS in cell aging. We choose the classic signaling pathway of cell aging (p19ARF/p53/p21Cip1) and prove that “FPS delays myocardial aging by stablizing telomere-telomerase system via p19ARF/p53/p21Cip1 pathway”.