4.5 Article

Salidroside protects human fibroblast cells from premature senescence induced by H2O2 partly through modulating oxidative status

期刊

MECHANISMS OF AGEING AND DEVELOPMENT
卷 131, 期 11-12, 页码 723-731

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.mad.2010.10.003

关键词

Salidroside; Cellular senescence; Oxidative stress; Antioxidant; DNA damage

资金

  1. Significant New Drug Development Science and Technology Major Projects of China [2009ZX09301-003]
  2. National Basic Research 973 Program of China [2007CB507406]
  3. Chinese Central and Non-profitable Basic R&D Funds for Scientific Research Institutes [IMBF200913]

向作者/读者索取更多资源

Although salidroside and salidroside-like compounds are considered as most critical constitutes needed and responsible for multiple therapeutic benefits of Rhodiola rosea L, including anti-aging, direct demonstration regarding the role of salidroside in anti-aging process is still deficient. In this study, we selected the H2O2-induced premature senescence model in human fetal lung diploid fibroblasts to investigate the protection of salidroside against aging in vitro and associated molecular mechanisms. We found that salidroside considerably reversed senescence-like phenotypes in the oxidant challenged model, including alterations of morphology, cell cycle. SA-beta-gal staining, DNA damage, as well as related molecules expression such as p53, p21 and p16. The protection occurred in a dose-dependent manner, with 5 mu M offering best efficacy. The proposed antioxidant property of the compound was confirmed in this cellular system, and thus at least partially accounted for the protection of the compound against premature senescence. Similar protection of salidroside against replicative senescence was observed as well. Interestingly, the regulation of senescence-related molecules by salidroside involved ROS-irrelevant mechanisms in both models. This finding presents salidroside as an attractive agent with potential to retard aging and attenuate age-related diseases in humans. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

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