T1-11, an adenosine derivative, ameliorates aging-related behavioral physiology and senescence markers in aging mice | Zendy

WeiHsiang Hsu | Zendy; YoungJi Shiao | Zendy; YenMing Chao | Zendy; Yi-Jeng Huang | Zendy; YunLian Lin | Zendy

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T1-11, an adenosine derivative, ameliorates aging-related behavioral physiology and senescence markers in aging mice

Author(s) -

WeiHsiang Hsu,

YoungJi Shiao,

YenMing Chao,

Yi-Jeng Huang,

YunLian Lin

Publication year - 2020

Publication title -

aging

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.473

H-Index - 90

ISSN - 1945-4589

DOI - 10.18632/aging.103279

Subject(s) - neurogenesis , senescence , adenosine , neurodegeneration , cognitive decline , brain aging , neuroscience , neuroinflammation , neuroprotection , aging brain , biology , dementia , pharmacology , medicine , chemistry , endocrinology , cognition , microbiology and biotechnology , inflammation , disease

Aging is a natural human process. It is uniquely individual, taking into account experiences, lifestyle habits and environmental factors. However, many disorders and syndromes, such as osteoporosis, neurodegenerative disorders, cognitive decline etc., often come with aging. The present study was designed to investigate the possible anti-aging effect of N 6 -(4-hydroxybenzyl)adenine riboside (T1-11), an adenosine analog isolated from Gastrodia elata , in a mouse model of aging created by D-galactose (D-gal) and the underlying mechanism, as well as explore the role of adenosine signaling in aging. T1-11 activated A 2A R and suppressed D-gal- and BeSO 4 -induced cellular senescence in vitro . In vivo results in mice revealed that T1-11 abated D-gal-induced reactive oxygen species generation and ameliorated cognitive decline by inducing neurogenesis and lowering D-gal-caused neuron death. T1-11 could be a potent agent for postponing senility and preventing aging-related neuroinflammation and neurodegeneration.

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