Abstract Title:

Salidroside protects human fibroblast cells from premature senescence induced by H(2)O(2) partly through modulating oxidative status.

Abstract Source:

Mech Ageing Dev. 2010 Nov-Dec;131(11-12):723-31. Epub 2010 Oct 28. PMID: 21035481

Abstract Author(s):

Gen-xiang Mao, Yan Wang, Qiang Qiu, Hong-bin Deng, Long-guo Yuan, Rui-guo Li, Dan-qing Song, Yi-yang Yvonne Li, Dian-dong Li, Zhen Wang

Article Affiliation:

Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences, Beijing 100050, People's Republic of China.


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 H(2)O(2)-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-β-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 5μM 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 findingpresents salidroside as an attractive agent with potential to retard aging and attenuate age-related diseases in humans.

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