葡萄糖胺通过激活有丝分裂在衰老大鼠中显示出强有力的热量限制模拟效应。

IF 2.2 4区 医学 Q3 GERIATRICS & GERONTOLOGY Rejuvenation research Pub Date : 2021-06-01 Epub Date: 2021-03-05 DOI:10.1089/rej.2020.2399
Raushan Kumar, Komal Saraswat, Syed Ibrahim Rizvi
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引用次数: 5

摘要

衰老与糖尿病、肥胖、心血管疾病和神经退行性疾病等几种非传染性疾病密切相关。葡萄糖胺(2-氨基-2-脱氧-d-葡萄糖,GlcN)是一种天然存在的氨基糖,据报道可作为热量限制模拟物(CRM)。在年轻和d-半乳糖诱导的加速衰老模型中,我们测试了持续口服膳食剂量的GlcN,并评估了红细胞和血浆中的各种衰老生物标志物。在glcn处理的年轻和加速衰老大鼠模型中,活性氧(ROS)显著增加。血浆铁还原能力(FRAP)、超氧化物歧化酶、过氧化氢酶和质膜氧化还原系统(PMRS)均有所增加。我们认为GlcN通过瞬间增加活性氧诱导促核分裂影响。我们的研究结果表明,GlcN可能是一个成功的客户关系管理。
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Glucosamine Displays a Potent Caloric Restriction Mimetic Effect in Senescent Rats by Activating Mitohormosis.

Aging is strongly correlated with several noncommunicable disorders such as diabetes, obesity, cardiovascular disease, and neurodegenerative conditions. Glucosamine (2-amino-2-deoxy-d-glucose, GlcN) is a naturally occurring amino sugar and is reported to act as a caloric restriction mimetic (CRM). In young and d-galactose-induced accelerated rat aging models, we tested a persistent oral dietary dose of GlcN and evaluated various aging biomarkers in erythrocytes and plasma. A significant increase in the reactive oxygen species (ROS) was observed in GlcN-treated young and accelerated senescent rat model. Increased value of ferric reducing ability of plasma (FRAP), superoxide dismutase, catalase, and plasma membrane redox system (PMRS) was observed. We suggest that GlcN induces a mitohormetic impact by a transient increase in ROS. Our findings indicate that GlcN may be a successful CRM.

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来源期刊
Rejuvenation research
Rejuvenation research 医学-老年医学
CiteScore
4.50
自引率
0.00%
发文量
41
审稿时长
3 months
期刊介绍: Rejuvenation Research publishes cutting-edge, peer-reviewed research on rejuvenation therapies in the laboratory and the clinic. The Journal focuses on key explorations and advances that may ultimately contribute to slowing or reversing the aging process, and covers topics such as cardiovascular aging, DNA damage and repair, cloning, and cell immortalization and senescence. Rejuvenation Research coverage includes: Cell immortalization and senescence Pluripotent stem cells DNA damage/repair Gene targeting, gene therapy, and genomics Growth factors and nutrient supply/sensing Immunosenescence Comparative biology of aging Tissue engineering Late-life pathologies (cardiovascular, neurodegenerative and others) Public policy and social context.
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