美國研究人員通過清除老化細(xì)胞讓小鼠青春常駐,，推遲顯現(xiàn)皺紋、肌肉萎縮,、白內(nèi)障等老化征兆,。
研究人員認(rèn)為，這一結(jié)果有望用于老年人護(hù)理,。專家稱,，這只是初步研究,，結(jié)果雖然“令人著迷”,，但須審慎看待。
緩衰老
研究主要針對(duì)老化細(xì)胞,。這種細(xì)胞不再分裂出新細(xì)胞,，在防止腫瘤生長方面起著重要作用。老化細(xì)胞由免疫系統(tǒng)清理,，隨著時(shí)間推移,，在身體積聚數(shù)量增多。研究人員估計(jì),，高齡老人全身大約10%的細(xì)胞為老化細(xì)胞,。
梅奧診所研究人員開發(fā)一種藥物，能夠殺死小鼠身上所有老化細(xì)胞,。研究人員首先通過基因工程培育特殊小鼠,，使它們的成熟老化速度快于正常同類,。
研究人員觀察三種老化征兆，即眼內(nèi)白內(nèi)障形成,、肌肉組織萎縮和皮下脂肪堆積,。結(jié)果發(fā)現(xiàn)，如果小鼠在老化跡象出現(xiàn)之前攝取藥物,，三種征兆“神奇地延遲”,；如果小鼠在老化跡象開始后攝取藥物，肌肉功能得到改善,。
不增壽
英國廣播公司（BBC）11月2日援引研究人員之一詹姆斯·柯克蘭的話報(bào)道：“我從未見過這樣的事,。”
另一研究人員揚(yáng)·范德烏森說：“我們對(duì)效果深感驚訝，它意義深遠(yuǎn),。”他對(duì)這種藥物的影響感到樂觀,，認(rèn)為這種藥有助老年人健康地度過晚年生活。在他看來,，“如果生活質(zhì)量差,，沒有人愿意長壽”。
這種藥物對(duì)小鼠沒有延年益壽的效果,。研究人員認(rèn)為，這可能因?yàn)樾∈蠼?jīng)過基因改造,。
研究結(jié)果由英國《自然》雜志發(fā)表,。
須審慎
這項(xiàng)研究結(jié)果向人們展示了延緩衰老的美好前景,，不過老化細(xì)胞無法完全清除,。
范德烏森說，年輕人能夠清除老化細(xì)胞,，“你須審慎看待可以強(qiáng)化免疫系統(tǒng),，確保老化細(xì)胞得到清理”；或者可以發(fā)明一種藥,，專門針對(duì)老化細(xì)胞,，因?yàn)檫@種細(xì)胞產(chǎn)生一種獨(dú)一無二的蛋白質(zhì)。
英國醫(yī)學(xué)研究委員會(huì)臨床學(xué)中心的吉澤斯·吉爾博士說,，梅奧診所研究人員的認(rèn)定需要“審慎對(duì)待,，這只是一項(xiàng)初步研究”。
他說,，不過這是一項(xiàng)“迷人”的研究,，顯示“如果能夠清除老化細(xì)胞，就可以改善老化帶來的（身體特征）表現(xiàn)型,，提高老齡人群生活質(zhì)量”,。（生物谷 Bioon.com）
doi:10.1038/nature10600
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Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
Darren J. Baker, Tobias Wijshake, Tamar Tchkonia, Nathan K. LeBrasseur, Bennett G. Childs, Bart van de Sluis, James L. Kirkland & Jan M. van Deursen
Advanced age is the main risk factor for most chronic diseases and functional deficits in humans, but the fundamental mechanisms that drive ageing remain largely unknown, impeding the development of interventions that might delay or prevent age-related disorders and maximize healthy lifespan. Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells1, 2. Senescent cells accumulate in various tissues and organs with ageing3 and have been hypothesized to disrupt tissue structure and function because of the components they secrete4, 5. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16Ink4a, to design a novel transgene, INK-ATTAC, for inducible elimination of p16Ink4a-positive senescent cells upon administration of a drug. Here we show that in the BubR1 progeroid mouse background, INK-ATTAC removes p16Ink4a-positive senescent cells upon drug treatment. In tissues—such as adipose tissue, skeletal muscle and eye—in which p16Ink4a contributes to the acquisition of age-related pathologies, life-long removal of p16Ink4a-expressing cells delayed onset of these phenotypes. Furthermore, late-life clearance attenuated progression of already established age-related disorders. These data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.
