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随着对端粒、端粒酶的结构和功能研究的深入,它们与衰老的关系日渐明确。自“端粒的缩短是启动衰老的分子钟”的假说提出后,大量实验结果都证明了该假说。尤其是人体hTRT细胞通过体外基因重组使端粒酶再表达实验,加入Asc 2P保持血管内皮细胞端粒酶活性并抑制氧化水平,从而延长细胞寿命实验,细胞因子IL-2、IL-4使T淋巴细胞成为持续细胞系并高表达端粒酶活性实验,不仅为该假说提供了有力证据,还开辟了一条较有前景的抗衰老的可能途径。
With the further study on the structure and function of telomere and telomerase, their relationship with aging is increasingly clear. Since the hypothesis that “telomere shortening is the molecular clock that initiates senescence”, a large number of experimental results have proved this hypothesis. In particular, human hTRT cells through in vitro gene recombination telomerase re-expression experiments, adding Asc 2P to maintain the vascular endothelial cell telomerase activity and inhibition of oxidation, thereby prolonging cell life experiments, cytokines IL-2, IL-4 T Lymphocytes become a continuous cell line and high expression of telomerase activity experiments, not only provide strong evidence for the hypothesis, but also opened up a more promising anti-aging possible ways.