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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >3 beta-Hydroxy-urs-12-en-28-oic Acid Modulates Dietary Restriction Mediated Longevity and Ameliorates Toxic Protein Aggregation in C. elegans
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3 beta-Hydroxy-urs-12-en-28-oic Acid Modulates Dietary Restriction Mediated Longevity and Ameliorates Toxic Protein Aggregation in C. elegans

机译：3β-羟基-URS-12-ZH-28-OIC酸调节膳食限制介导的寿命和改善秀丽隐杆线的毒性蛋白质聚集

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Species from lower invertebrates to a spectrum of mammals show antiaging health benefits of phytochemical(s). Here, we explored the prolongevity effects of a natural triterpenoid, ursolic acid (3 beta-hydroxy-urs-12-en-28-oic acid; UA) in Caenorhabditis elegans with maximal life span being evident at 25 mu M UA. Similar to eat-2 mutants, UA uptake by worm results in reduced fat storage and attenuation of reactive oxygen species (ROS), independent of superoxide dismutase(s) activation. The genetic requirements for UA-mediated longevity are quite similar to dietary restriction (DR) achieved through SKN-1/NRF-2 exhibiting upregulation of downstream target genes gcs-1 and daf-9. Longevity mechanism was independent of PHA-4/FOXA and attributed to partial dependence on sir-2.1. Altogether, our study suggests differential use of UA-elicited signaling cascades in nutrient sensing for longevity. Both the redox state and the proteostasis of an organism play critical role in aging and disease resistance. Interestingly, we observed a reduction of toxic protein aggregation in transgenic polyglutamine (polyQ) C. elegans model and UA-mediated JNK-1 (c-Jun-NH2-terminal kinase) activation in wild-type animals. Thus, our study demonstrates a small extent of prevention against proteotoxic stress by UA coupled with positive aspects of DR-mediated longevity.
机译：从下穷无脊椎动物到哺乳动物的谱的物种显示植物化学的抗衰率健康益处。在这里，我们探讨了天然三萜类化合物（3β-羟基-URS-12-烯-22- oIc酸; uA）在Caenorhabditis elegans中的增殖效应，最大的寿命在25 mu m ua处显而易见。类似于吃-2突变体，UA通过蠕虫的吸收导致反应性氧物种（ROS）的脂肪储存和衰减，与超氧化物歧化酶的活化无关。 UA介导的寿命的遗传要求与通过SKN-1 / NRF-2实现的膳食限制（DR）非常相似，所述SKN-1 / NRF-2表现出下游靶基因GCS-1和DAF-9的上调。寿命机制与PHA-4 / FOXA无关，并归因于部分依赖SIR-2.1。完全是，我们的研究表明，UA引发的信号级联在营养传感中的差异使用寿命，用于寿命。氧化还原状态和生物体的蛋白质都在衰老和抗病抗性方面发挥着关键作用。有趣的是，在野生型动物中观察到转基因聚谷氨酰胺（PolyQ）C.秀丽杆菌模型和UA介导的JNK-1（C-JUN-NH2-末端激酶）活化的有毒蛋白质聚集的减少。因此，我们的研究表明，UA与博士介导的寿命的积极方面相结合了对蛋白毒性应力的小程度。

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