人們?cè)缫阎?，限制卡路里攝入是延長(zhǎng)有機(jī)體壽命的好方法。美國(guó)科學(xué)家近日研究發(fā)現(xiàn)，抗抑郁藥脫爾煩（Tolvon）具有同樣的功效，它能夠?qū)⑿沱愲[桿線蟲（Caenorhabditis elegans）的壽命延長(zhǎng)三分之一以上,，即從三周延長(zhǎng)到四周多。這為研究人類的抗老化問題提供了重要的參考,。相關(guān)論文11月22日發(fā)表于《自然》（Nature）雜志上,。
領(lǐng)導(dǎo)此次研究的是美國(guó)佛瑞德·哈金森癌癥研究中心(Fred Hutchinson Cancer Research Center)的分子生物學(xué)家Linda Buck。她和同事花了5年的時(shí)間,，從8.8萬種化學(xué)制劑中挑選出了100多種,，它們能夠延長(zhǎng)秀麗隱桿線蟲的壽命。由于對(duì)這些制劑在生物體內(nèi)的反應(yīng)機(jī)理并不清楚,，她們轉(zhuǎn)而尋找具有相似作用的成品藥物。結(jié)果發(fā)現(xiàn),，抗抑郁藥脫爾煩能夠?qū)⑦@種線蟲的壽命延長(zhǎng)三分之一以上,。
實(shí)驗(yàn)中脫爾煩并沒有使秀麗隱桿線蟲的進(jìn)食量減少，這表明它并不是通過實(shí)際降低卡路里攝入來延長(zhǎng)壽命的,。Buck說：“它們看起來很活躍,，并不像非常饑餓的樣子。”不過研究人員相信,，脫爾煩延長(zhǎng)壽命的機(jī)制與卡路里限制是一樣的,，即脫爾煩誘騙線蟲大腦相信攝入了較少的卡路里，從而幫助延長(zhǎng)了機(jī)體壽命,。
美國(guó)哈佛大學(xué)的生物學(xué)家David Sinclair認(rèn)為,，對(duì)于人類的老化問題研究來說，找到能夠延長(zhǎng)線蟲壽命的藥物是重要的第一步,。
不過Buck提醒說,，她反對(duì)僅僅利用其小組的初步成果就預(yù)測(cè)，人類能從脫爾煩中得到相同的好處,。下一步她和研究小組計(jì)劃在小鼠身上進(jìn)行類似實(shí)驗(yàn),，并且將更深入地研究已發(fā)現(xiàn)的100多種化學(xué)制劑，以探尋動(dòng)物老化的原因及減緩這一過程的方法,。（科學(xué)網(wǎng) 梅進(jìn)/編譯）
原始出處:
Nature 450, 553-556 (22 November 2007) | doi:10.1038/nature05991; Received 31 July 2007; Accepted 11 October 2007
An antidepressant that extends lifespan in adult Caenorhabditis elegans
Michael Petrascheck1, Xiaolan Ye1 & Linda B. Buck1
Howard Hughes Medical Institute, Basic Sciences Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, Washington 98109-1024, USA
Correspondence to: Linda B. Buck1 Correspondence and requests for materials should be addressed to L.B.B. (Email: [email protected]).
Abstract
The mechanisms that determine the lifespan of an organism are still largely a mystery1. One goal of ageing research is to find drugs that would increase lifespan and vitality when given to an adult animal. To this end, we tested 88,000 chemicals for the ability to extend the lifespan of adult Caenorhabditis elegans nematodes. Here we report that a drug used as an antidepressant in humans increases C. elegans lifespan. In humans, this drug blocks neural signalling by the neurotransmitter serotonin. In C. elegans, the effect of the drug on lifespan is reduced or eradicated by mutations that affect serotonin synthesis, serotonin re-uptake at synapses, or either of two G-protein-coupled receptors: one that recognizes serotonin and the other that detects another neurotransmitter, octopamine. In vitro studies show that the drug acts as an antagonist at both receptors. Testing of the drug on dietary-restricted animals or animals with mutations that affect lifespan indicates that its effect on lifespan involves mechanisms associated with lifespan extension by dietary restriction. These studies indicate that lifespan can be extended by blocking certain types of neurotransmission implicated in food sensing in the adult animal, possibly leading to a state of perceived, although not real, starvation.
