Bisdemethoxycurcumin Increases Sirt1 to Antagonize t-BHP-Induced Premature Senescence in WI38 Fibroblast Cells

Curcuminoids are well known for their capabilities to combat risk factors that are associated with ageing and cellular senescence. Recent reports have demonstrated that curcuminoids can extend the lifespan of model organisms. However, the underlying mechanisms by which these polyphenic compounds exe...

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Published in:Evidence-based complementary and alternative medicine 2013-01, Vol.2013 (2013), p.1-9
Main Authors: Li, Ying-Bo, Zhong, Zhang-Feng, Chen, Mei-Wan, Bao, Jiao-Lin, Wu, Guo-Sheng, Zhang, Qing-Wen, Lee, Simon Ming-Yuen, Hoi, Pui-Man, Wang, Yi-Tao
Format: Article
Language:English
Subjects:
Aging
Alzheimer's disease
Cancer
Fibroblasts
Galactosidase
Gene expression
Kinases
Life span
Nicotianamine
Oxidative stress
Polyphenols
Potassium
Proteins
Retina
Retinoblastoma
Retinoblastoma protein
Risk factors
Senescence
Signal transduction
siRNA
SIRT1 protein
Substance abuse treatment
β-Galactosidase
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Summary:Curcuminoids are well known for their capabilities to combat risk factors that are associated with ageing and cellular senescence. Recent reports have demonstrated that curcuminoids can extend the lifespan of model organisms. However, the underlying mechanisms by which these polyphenic compounds exert these beneficial effects remain unknown. In this study, t-BHP-induced premature senescence model in human fibroblasts was chosen to explore the protective effects of a curcuminoid, bisdemethoxycurcumin (BDMC), on cellular senescence. The results demonstrated that BDMC attenuated oxidative stress-induced senescence-like features which include the induction of an enlarged cellular appearance, higher frequency of senescence-associated β-galactosidase staining activity, appearance of senescence-associated heterochromatic foci in nuclei, decrease in proliferation capability, and alteration in related molecules such as p16 and retinoblastoma protein. Notably, we found that BDMC treatment activated Sirt1/AMPK signaling pathway. Moreover, downregulating Sirt1 by the pharmacological inhibitor nicotianamine or small interfering RNA blocked BDMC-mediated protection against t-BHP-mediated decrease in proliferation. These results suggested that BDMC prevented t-BHP-induced cellular senescence, and BDMC-induced Sirt1 may be a mechanism mediating its beneficial effects.
ISSN:1741-427X
1741-4288
DOI:10.1155/2013/851714