Caffeine Protects Skin from Oxidative Stress-Induced Senescence through the Activation of Autophagy

Skin cells are vulnerable to oxidative stress-induced senescence, which may lead to abnormal aging or aging-related disorders. Therefore, strategies that can ameliorate oxidative stress-induced senescence are expected to protect skin from damage, holding the promise of treating skin diseases in the...

Full description

Saved in:
Bibliographic Details
Published in:Theranostics 2018-01, Vol.8 (20), p.5713-5730
Main Authors: Li, Yi-Fang, Ouyang, Shu-Hua, Tu, Long-Fang, Wang, Xi, Yuan, Wei-Lin, Wang, Guo-En, Wu, Yan-Ping, Duan, Wen-Jun, Yu, Hong-Min, Fang, Zhong-Ze, Kurihara, Hiroshi, Zhang, Youwei, He, Rong-Rong
Format: Article
Language:English
Subjects:
Aging - pathology
Amidines - toxicity
Animals
Antioxidants - administration & dosage
Autophagy - drug effects
Caffeine - administration & dosage
Cells, Cultured
Disease Models, Animal
Humans
Mice
Models, Theoretical
Oxidants - toxicity
Oxidative Stress
Research Paper
Skin - drug effects
Skin - radiation effects
Skin Diseases - pathology
Skin Diseases - prevention & control
Treatment Outcome
Ultraviolet Rays
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Skin cells are vulnerable to oxidative stress-induced senescence, which may lead to abnormal aging or aging-related disorders. Therefore, strategies that can ameliorate oxidative stress-induced senescence are expected to protect skin from damage, holding the promise of treating skin diseases in the clinic. This study aims to investigate whether caffeine, a well-known purine alkaloid, is able to prevent skin from oxidative stress-induced senescence, and to explore the underlying molecular mechanisms. : A free radical inducer 2,2'-Azobis (2-amidinopropane) dihydrochloride (AAPH) was used to induce oxidative stress and cellular senescence in both transformed skin cells and in normal human epidermal keratinocytes (NHEKs). Ultraviolet (UV) irradiation was established as the oxidative stress model in mouse skin tissues. Cellular senescence was determined by SA β-galactosidase staining, immunofluorescence and western blotting. Activation of autophagy was confirmed by western blotting, immunofluorescence, and transmission electron microscopy. Reactive oxygen species (ROS) detection by commercial kits, gene knockdown by RNA interference (RNAi) and receptor activation/inactivation by agonist/antagonist treatment were applied in mechanistic experiments. : We report that AAPH induced senescence in both transformed skin cells and in NHEKs. Similarly, UV irradiation induced senescence in mouse skin tissues. Remarkably, low dose of caffeine (
ISSN:1838-7640
1838-7640
DOI:10.7150/thno.28778