限食分子机制的研究进展.docVIP

  限食分子机制的研究进展 郑全喜，王昆，刘超** （江苏省中西医结合医院内分泌科，南京，210028） 5 10 摘要：限食可有效抑制衰老相关疾病的发生，在大量动物模型的研究中被认为是延长平均及 最长寿命最有效的干预手段。目前限食的机制尚不明确，主要有抗逆性假说，氧化应激假说 和节俭假说等三种假说。而对限食的细胞及分子水平作用机制研究主要集中在单细胞生物和 啮齿类动物。目前一致认为，限食可以调控氧化应激、内质网应激、与细胞生长衰老相关的 信号通路（mTOR、AMPK）、细胞凋亡、自噬以及代谢等途径。科学界对限食延缓衰老和 抑制衰老相关疾病发生的认识还处于初级阶段，因此关于限食条件下各种信号转导途径的研 究有待进一步深入。 关键词：限食；氧化应激；凋亡；自噬 中图分类号：R58 15 Advanced on the mechanism of caloric restriction ZHEGN Quanxi, WANG Kun, LIU Chao (Department of Endocrinology and Metabolism, Jiangsu Province Hospital on Integration of 20 25 30 35 40 Chinese and Western Medicine, Nan-jing, 210028) Abstract: In a number of studies of animal models, caloric restriction is thought to be the most effective means of intervention of extending the average and the longest life, and also can effectively inhibit the development of the age-related diseases. The mechanism of caloric restriction is not clear, and there are three hypotheses, including the stress resistance hypothesis, the oxidative stress hypothesis and thrift hypothesis. The investigations of the cellular and molecular mechanism of caloric restriction mainly focus on the unicellular organisms and rodent animals. There is a consensus that caloric restriction can regulate oxidative stress, endoplasmic reticulum stress, cell growth and senescence associated signaling pathway (such as mTOR, AMPK), cell apoptosis, autophagy and metabolism. While the understanding of scientific community on delaying senescence and preventing aging related diseases of caloric restriction is still in the initial stage, further studies of various signal transduction pathways under caloric restriction conditions are still required. Key words: Caloric restriction; Oxidative stress; Apoptosis, Autophagy 0 引言 大量动物模型的研究已经表明，限食是延长平均及最长寿命最有效的干预手 段。限食可有效抑制如脑血管、高血压等衰老相关疾病的发生[1,2,3]。目前限食的 机制尚不明确，主要有三种假说：抗逆性假说，氧化应激假说和节俭假说。而限 食细胞及分子水平的作用机制主要集中在单细胞生物和啮齿类动物。目前一致认 为，限食可以调控氧化应激、内质网应激、与细胞生长衰老相关的信号通路 （mTOR、AMPK）、细胞凋亡和自噬以及代谢等途径。本文主要从限食与氧化 作者简介：郑全喜（1985-），男，研究实习员，主要从事内分泌代谢