论文部分内容阅读
生物衰老是自然界一种复杂的生命现象。生物学家对生物衰老的机制作了许多推测,提出了衰老的自由基学说、突变学说、DNA损伤修复学说及遗传学说等等。尽管这些学说各自都获得一些实验证据的支持,但至今仍不能用一种学说全面地解释衰老的现象。随着分子生物学的迅猛发展,衰老的机制研究已深入到分子水平。 个体的衰老是各脏器衰老的总和。细胞衰老时增生能力的下降可能是器官衰老的基本过程之一。在正常细胞培养条件下,成纤维细胞（fibroblast,Fb）具有有限的生长增殖能力。这一事实已被众多的学者所接受并把这一模型系统广泛地应用于细胞水平的衰老研究中。
Biological aging is a complex phenomenon in nature. Biologists made a lot of speculations about the mechanism of biological aging, and proposed the free radical theory of senescence, the mutation theory, the theory of DNA damage repair and the theory of genetics. Although each of these doctrines is supported by some experimental evidence, it is still not possible to explain the phenomenon of aging in a comprehensive way. With the rapid development of molecular biology, the mechanism of aging has been deep into the molecular level. Individual aging is the sum of aging organs. The decline of hyperplasia in cellular aging may be one of the basic processes of organ aging. Under normal cell culture conditions, fibroblasts (Fbs) have limited ability to proliferate. This fact has been accepted by many scholars and the model system is widely used in cell-level aging research.