蘋果皮提取物可延緩衰老進(jìn)程
“一天一蘋果，醫(yī)生遠(yuǎn)離你”是一句耳熟能詳?shù)慕】抵V語(yǔ)。不過，吃蘋果的最好方法是帶皮吃。據(jù)最新一期《自然—醫(yī)學(xué)》（Nature Medicine）報(bào)道，美國(guó)科研人員發(fā)現(xiàn)，達(dá)沙替尼（一種白血病藥物）和槲皮素（一種來自蘋果皮的提取物）的組合可使老年小鼠的壽命延長(zhǎng)36%。
衰老細(xì)胞通常在60多歲時(shí)出現(xiàn)在人體內(nèi)，而在肥胖人群或慢性病患者體內(nèi)出現(xiàn)得更早。這些異常細(xì)胞處于衰退狀態(tài)，但其又不甘于死亡。有人認(rèn)為，衰老細(xì)胞本身會(huì)催化衰老進(jìn)程。
美國(guó)梅奧診所詹姆斯·柯克蘭領(lǐng)導(dǎo)的研究團(tuán)隊(duì)證明，情況確實(shí)如此。當(dāng)研究人員向6個(gè)月大的小鼠注射少量衰老細(xì)胞時(shí)，它們的速度、耐力和力量在幾周內(nèi)下降了20%至50%，差不多是典型2歲老年小鼠的水平。
為了阻斷衰老細(xì)胞的影響，研究團(tuán)隊(duì)選擇了達(dá)沙替尼和槲皮素的組合，因?yàn)閮烧叨紩?huì)干擾衰老細(xì)胞避免死亡的方式。當(dāng)研究團(tuán)隊(duì)將組合藥物給予因注入衰老細(xì)胞而老化的幼鼠時(shí)，這些小鼠所失去的身體能力在兩周內(nèi)恢復(fù)了50%至100%。
當(dāng)研究團(tuán)隊(duì)將藥物給予年齡在24至27個(gè)月間的老年小鼠時(shí)，這些小鼠的速度、耐力和力量提高了30%到100%，而且它們的剩余壽命要比那些未給藥老年小鼠長(zhǎng)36%。（來源：科技日?qǐng)?bào)?馮衛(wèi)東）
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Senolytics improve physical function and increase lifespan in old age
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Abstract??Physical function declines in old age, portending disability, increased health expenditures, and mortality. Cellular senescence, leading to tissue dysfunction, may contribute to these consequences of aging, but whether senescence can directly drive age-related pathology and be therapeutically targeted is still unclear. Here we demonstrate that transplanting relatively small numbers of senescent cells into young mice is sufficient to cause persistent physical dysfunction, as well as to spread cellular senescence to host tissues. Transplanting even fewer senescent cells had the same effect in older recipients and was accompanied by reduced survival, indicating the potency of senescent cells in shortening health- and lifespan. The senolytic cocktail, dasatinib plus quercetin, which causes selective elimination of senescent cells, decreased the number of naturally occurring senescent cells and their secretion of frailty-related proinflammatory cytokines in explants of human adipose tissue. Moreover, intermittent oral administration of senolytics to both senescent cell–transplanted young mice and naturally aged mice alleviated physical dysfunction and increased post-treatment survival by 36% while reducing mortality hazard to 65%. Our study provides proof-of-concept evidence that senescent cells can cause physical dysfunction and decreased survival even in young mice, while senolytics can enhance remaining health- and lifespan in old mice.