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Estudio2018Solo mecanismosAcceso abierto

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

Li YF, Ouyang SH, Tu LF, Wang X, Yuan WL, Wang GE, Wu YP, Duan WJ, Yu HM, Fang ZZ, Kurihara H, Zhang Y, He RR

Theranostics · 155 citas

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Solo mecanismos

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Cómo se estudió

Diseño
Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
Estudiado en
Células o muestras de laboratorio
Resultado principal
Solo mecanismos

Quién lo pagó

Financiación
Financiación independiente
Gobierno
National Cancer Institute
Gobierno
NCI NIH HHS
Subvenciones
National Cancer Institute (R01-CA230453)

Según 2 financiadores declarados y la declaración de financiación del texto completo.

Publicación

Publicado
2018-01-01 · Theranostics · vol. 8 · número 20 · págs. 5713–5730
Editorial
Ivyspring International Publisher
Citado
202 citas · más que el 98% de estudios similares · 6.8× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
77 trabajos
Acceso
Acceso abierto (revista) · CC-BY-NC
Áreas de investigación
Sirtuins and Resveratrol in Medicine · Autophagy in Disease and Therapy · Skin Protection and Aging
Palabras clave
Oxidative stress, Senescence, Reactive oxygen species, Autophagy, Caffeine, Cell biology, Chemistry, Gene knockdown, Biology, Biochemistry, Apoptosis
MeSH
cells, cultured, skin, animals, humans, mice, skin diseases, disease models, animal, amidines, caffeine, antioxidants, oxidants, treatment outcome, ultraviolet rays, oxidative stress, aging, models, theoretical, autophagy

13 autores

  • Yifang Li🇨🇳Jinan University
  • Shu‐Hua Ouyang🇨🇳Jinan University
  • Long‐Fang Tu🇨🇳Jinan University
  • Xi Wang🇨🇳Jinan University
  • Wei‐Lin Yuan🇨🇳Jinan University
  • Guo-En Wang🇨🇳Jinan University
  • Yanping Wu🇨🇳Jinan University
  • Wen‐Jun Duan🇨🇳Jinan University
  • Hong-Min Yu🇨🇳Jinan University
  • Zhong‐Ze Fang🇨🇳Tianjin Medical University
  • Hiroshi Kurihara🇨🇳Jinan University
  • Youwei Zhang🇺🇸Case Western Reserve University
  • Rong‐Rong He🇨🇳Jinan University

Resumen

El texto original del estudio, en el idioma en que se publicó.

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. Methods: 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 in vivo 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. Results: 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 (Conclusion: The results reveal that caffeine protects skin from oxidative stress-induced senescence through activating the A2AR/SIRT3/AMPK-mediated autophagy. Our study not only demonstrated the beneficial effect of caffeine using both in vitro and in vivo models, but also systematically investigated the underlying molecular mechanisms. These discoveries implicate the potential of caffeine in the protection of skin disease.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY-NC).

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