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Research Paper|Volume 12, Issue 11|pp 10556—10577

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

Wei-Hsiang Hsu1, Young-Ji Shiao2,3, Yen-Ming Chao1, Yi-Jeng Huang1, Yun-Lian Lin1,4
  • 1Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung 40402, Taiwan
  • 2National Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei 11221, Taiwan
  • 3Institute of Biopharmaceutical Science, National Yang-Ming University, Taipei 112, Taiwan
  • 4Department of Pharmacy, National Taiwan University, Taipei 10050, Taiwan
* Equal contribution
Received: May 27, 2019Accepted: April 20, 2020Published: June 5, 2020
https://doi.org/10.18632/aging.103279

Copyright © 2020 Hsu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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 N6-(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 A2AR and suppressed D-gal- and BeSO4-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.