一项最新研究指出，家庭小药箱里常备的维生素C或许能治疗可加速衰老的紊乱，尤其是成人早衰症(Werner's syndrome)，这项研究成果发表在2010年1月的《美国实验生物学会联合会杂志》上。
加拿大科研组在这份科研报告中指出，维生素C阻止甚至逆转了患成人早衰症的老鼠的加速衰老过程，不过这项发现或许还适用于其它早衰症。患有成人早衰症的人，从20多岁开始表现出加速衰老的迹象，在50岁之前形成老年性疾病，他们一般会在50岁之前死亡。这篇论文的联合作者，加拿大魁北克的迈克勒贝尔说：“我们的研究显然说明，没患有疾病的健康生物或个体，不必通过服用大量维生素C来延长寿命，尤其当他们拥有均衡饮食，并经常进行锻炼时。当生物或个体拥有WRN 基因变种，或者任何受WRN蛋白影响的基因时，他们倾向于患老年性疾病，这些人服用一定数量的维生素C会给健康带来好处。”
科学家在健康老鼠和携带可引发成人早衰症(WRN基因)基因变种的老鼠的饮水里加入了维生素C。在进行治疗前，携带WRN基因变种的老鼠更易发胖、患糖尿病，并会慢慢形成心脏病和癌症。进行治疗后，携带突变基因的老鼠变得跟正常老鼠一样健康，寿命期限达到正常水平。维生素C还促进了老鼠储存和燃烧脂肪的能力，减少了组织炎症，并降低了携带WRN基因的老鼠的氧化应激。健康老鼠没表现出从维生素C受益的迹象。
《美国实验生物学会联合会杂志》的总编辑杰拉尔德威斯曼说：“维生素C已经成为我们药箱和食品中被人误解最深的物质，这项研究和其他类似研究有助于解释，这种化学物质是如何帮助一些人而不是所有人预防早衰，以及帮助他们预防早衰的原因。”
推荐原始出处：
The FASEB Journal. 2010;24:158-172. doi: 10.1096/fj.09-137133.
Vitamin C restores healthy aging in a mouse model for Werner syndrome
Laurent Massip*, Chantal Garand*, Eric R. Paquet*, Victoria C. Cogger, Jennifer N. O'Reilly, Leslee Tworek, Avril Hatherell, Carla G. Taylor, Eric Thorin, Peter Zahradka, David G. Le Couteur and Michel Lebel*,1
Werner syndrome (WS) is a premature aging disorder caused by mutations in a RecQ-like DNA helicase. Mice lacking the helicase domain of the WRN homologue exhibit many phenotypic features of WS, including a prooxidant status and a shorter mean life span compared to wild-type animals. Here, we show that Wrn mutant mice also develop premature liver sinusoidal endothelial defenestration along with inflammation and metabolic syndrome. Vitamin C supplementation rescued the shorter mean life span of Wrn mutant mice and reversed several age-related abnormalities in adipose tissues and liver endothelial defenestration, genomic integrity, and inflammatory status. At the molecular level, phosphorylation of age-related stress markers like Akt kinase-specific substrates and the transcription factor NF-B, as well as protein kinase C and Hif-1 transcription factor levels, which are increased in the liver of Wrn mutants, were normalized by vitamin C. Vitamin C also increased the transcriptional regulator of lipid metabolism PPAR. Finally, microarray and gene set enrichment analyses on liver tissues revealed that vitamin C decreased genes normally up-regulated in human WS fibroblasts and cancers, and it increased genes involved in tissue injury response and adipocyte dedifferentiation in obese mice. Vitamin C did not have such effect on wild-type mice. These results indicate that vitamin C supplementation could be beneficial for patients with WS.―Massip, L., Garand, C., Paquet, E. R., Cogger, V. C., O'Reilly, J. N., Tworek, L., Hatherell, A., Taylor, C. G., Thorin, E., Zahradka, P., Le Couteur, D. G., Lebel, M. Vitamin C restores healthy aging in a mouse model for Werner syndrome.
