Echinacoside, a phenylethanoid glycoside from Cistanche deserticola, extends lifespan of Caenorhabditis elegans and protects from Aβ-induced toxicity
Echinacoside, a phenylethanoid glycoside from Cistanche deserticola, extends lifespan of Caenorhabditis elegans and protects from Aβ-induced toxicity
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Echinacoside 是一种来自肉苁蓉的苯乙醇苷，可延长秀丽隐杆线虫的寿命并防止 A β 诱导的毒性
DOI：
10.1007/s10522-017-9738-0
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发表时间：
2018-02-01
期刊：
影响因子：
4.5
通讯作者：
Wang, Hong-Bing
中科院分区：
文献类型：
--
作者：
Chen, Wei;Lin, Hong-Ru;Wang, Hong-Bing
肉苁蓉已被发现对衰老和与年龄有关的疾病发挥保护作用，但其长寿效应的机制仍不清楚。在这里，多细胞模式生物秀丽隐杆线虫被用于鉴定松果菊苷（ECH）（一种从秀丽隐杆线虫中分离的苯乙醇苷）对延长寿命和对抗β-淀粉样蛋白（A β）诱导的毒性的保护作用。沙漠生。我们的研究结果表明，ECH延长了蠕虫的平均寿命，并增加了它们在氧化应激下的存活率。细胞内活性氧的水平和脂肪的积累也显着抑制ECH。此外，ECH介导的寿命延长被发现依赖于mev-1，eat-2，daf-2和daf-16，而不是sir-2.1或hsf-1基因。此外，ECH触发了α-16的核定位，并上调了其下游靶点sod-3和hsp-16.2。此外，ECH显着提高CL 4176蠕虫的生存率，以应对A β蛋白聚集诱导的蛋白毒性应激。总的来说，这些研究结果表明，活性氧清除，饮食限制，胰岛素/胰岛素样生长因子信号通路可能部分参与ECH介导的寿命延长。因此，ECH可能靶向多种长寿机制以延长寿命，并具有预防阿尔茨海默病进展的潜力。
Cistanche deserticola has been found to exert protection against aging and age-related diseases, but mechanisms underlying its longevity effects remain largely unclear. Here, the multicellular model organism Caenorhabditis elegans was employed to identify lifespan extending and protective effects against beta-amyloid (A beta) induced toxicity by echinacoside (ECH), a phenylethanoid glycoside isolated from C. deserticola. Our results showed that ECH extends the mean lifespan of worms and increases their survival under oxidative stress. Levels of intracellular reactive oxygen species and fat accumulation were also significantly suppressed by ECH. Moreover, ECH-mediated lifespan extension was found to be dependent on mev-1, eat-2, daf-2, and daf-16, but not sir-2.1 or hsf-1 genes. Furthermore, ECH triggered DAF-16 nuclear localization and upregulated two of its downstream targets, sod-3 and hsp-16.2. In addition, ECH significantly improved the survival of CL4176 worms in response to proteotoxic stress induced by A beta protein aggregation. Collectively, these findings suggested that reactive oxygen species scavenging, dietary restriction, and insulin/insulin-like growth factor signaling pathways could be partly involved in ECH-mediated lifespan extension. Thus, ECH may target multiple longevity mechanisms to extend lifespan and have a potency to prevent Alzheimer's disease progression.