Journal
MECHANISMS OF AGEING AND DEVELOPMENT
Volume 175, Issue -, Pages 1-6Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mad.2017.12.005
Keywords
Salidroside; Inflammatory cytokines; SIRT3; Endothelial cellular senescence
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Funding
- Technology Bureau of Chengdu [2015-HM01-00434-SF, 2015-HM01-00580-SF]
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Objective: Endothelial cellular senescence is an important contributor to the endothelial dysfunction and atherosclerosis. Our previous studies suggested that salidroside (SAL) can alleviate atherosclerosis and protect endothelial cells against oxidative stress induced damage. However, the effect and mechanism of SAL on endothelial cellular senescence is still unclear. Here, we investigated the underlying mechanisms of SAL on preventing endothelial cellular premature senescence. Methods and results: We established a hyperhomocysteinemia (HHcy)mouse model via high methionine diet (HMD) to explore the protective effect of SAL. According to our results, the HMD elevated the concentration of serum homocysteine. HHcy induced the collagen deposition and the up-regulation of senescence markers, i.e. p16(INK4A) and p21(CIP1), in intima-medial of aorta. In addition, SAL also inhibited the expression of CD68 and intercellular adhesion molecule 1 (ICAM1) in aorta. In senescent human umbilical vein endothelial cells (HUVECs) induced by H2O2, SAL treatment alleviated the expression of p16(INK4A) and p21(CI)(P1) and reduced the activity of senescence-associated (SA)-beta-gal. Conclusion: our data suggested that SAL decreased the expression of inflammatory cytokines and up-regulated the expression of SIRT3, which might be the underlying mechanism of SAL on preventing endothelial cells from premature senescence.
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