Inhibitory effect of vitamin C on intrinsic aging in human dermal fibroblasts and hairless mice

Vitamin C significantly reduced senescence-associated β-galactosidase (SA-β-gal) activity, with both the suppression of cell-cycle inhibitors (p53, p21, p16, and pRb) and stimulation of cell-cycle activators (E2F1 and E2F2). Vitamin C also effectively attenuated the hyperactivation of the phosphatid...

Full description

Saved in:
Bibliographic Details
Published inFood science and biotechnology Vol. 27; no. 2; pp. 555 - 564
Main Authors Jeong, Jae-Hong, Kim, Mi-Bo, Kim, Changhee, Hwang, Jae-Kwan
Format Journal Article
LanguageEnglish
Published Singapore Springer Singapore 01.04.2018
Springer Nature B.V
한국식품과학회
Subjects
Online AccessGet full text
ISSN1226-7708
2092-6456
2092-6456
DOI10.1007/s10068-017-0252-6

Cover

More Information
Summary:Vitamin C significantly reduced senescence-associated β-galactosidase (SA-β-gal) activity, with both the suppression of cell-cycle inhibitors (p53, p21, p16, and pRb) and stimulation of cell-cycle activators (E2F1 and E2F2). Vitamin C also effectively attenuated the hyperactivation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase-B (AKT) signaling pathway. The expression of the longevity marker, the mammalian target of rapamycin (mTOR), was down-regulated by vitamin C while the expressions of forkhead box O3a (FoxO3a) and sirtuin1 (SIRT1) were up-regulated by vitamin C. In the middle-aged (MA) mice, oral administration of vitamin C significantly inhibited wrinkle formation, skin atrophy, and loss of elasticity through increasing collagen and elastic fiber. The increase in transepidermal water loss and the decrease in skin hydration were recovered by vitamin C treatment in the MA mice. Overall, vitamin C effectively prevents cellular senescence in vitro and in vivo suggesting it has protective potential against natural aging of the skin.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ISSN:1226-7708
2092-6456
2092-6456
DOI:10.1007/s10068-017-0252-6