Repositorio Institucional
Repositorio Institucional
CONICET Digital
  • Inicio
  • EXPLORAR
    • AUTORES
    • DISCIPLINAS
    • COMUNIDADES
  • Estadísticas
  • Novedades
    • Noticias
    • Boletines
  • Ayuda
    • General
    • Datos de investigación
  • Acerca de
    • CONICET Digital
    • Equipo
    • Red Federal
  • Contacto
JavaScript is disabled for your browser. Some features of this site may not work without it.
  • INFORMACIÓN GENERAL
  • RESUMEN
  • ESTADISTICAS
 
Artículo

Metformin inhibits the inflammatory and oxidative stress response induced by skin UVB-irradiation and provides 4-hydroxy-2-nonenal and nitrotyrosine formation and p53 protein activation

Pinheiro Souza Neto, Fernando; Marinello, Poliana Camila; Melo, Gabriela Pasqual; Zambeli Naira Ramalho, Leandra; Cela, Eliana M.; Campo, Valeria EvelynIcon ; Gonzalez Maglio, Daniel HoracioIcon ; Cecchini, Rubens; Lourenço Cecchini, Alessandra
Fecha de publicación: 11/2020
Editorial: Elsevier Ireland
Revista: Journal of Dermatological Science
ISSN: 0923-1811
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Farmacología y Farmacia

Resumen

Skin exposure to ultraviolet B (UVB) radiation leads to local oxidative stress, inflammation, systemic immunosuppression and, ultimately, the development of skin cancer. Metformin is the most prescribed drug for type 2 diabetes, and it has been shown that chronic treatments with this drug reduces skin cancer incidence.Objective. Our aim was to analyze the effects of metformin on UVB-induced acute local damage.Methods. C57/BL6 mice were pretreated with 90 mg/kg of metformin for 11 days and exposed to 400 mJ/cm2 of UVB radiation. Twenty-four hours later, we obtained skin samples to determine oxidative stress and the inflammatory response. Results. We observed that metformin did not prevent UVB-induced epidermal damage, Langerhans cells loss or mitochondrial alterations in epidermal cells. However, it improved the reducing state in the skin, increasing antioxidant molecules that led to reduced 4-hidroxynonenal and nitrotyrosine labeling. Local inflammatory mediators increased by UVB radiation, such as IL-6 and IL-1β, were also reduced by metformin.Conclusion. We demonstrated that metformin reduces UVB-induced local and systemic damage, changes that could explain its antitumoral effect. Thus, the use of metformin as a potential agent to maintain skin homeostasis and prevent UVB-induced lesions requires evaluation.
Palabras clave: METFORMIN , OXIDATIVE STRESS , SKIN IMMUNE RESPONSE , UVB SKIN DAMAGE
Ver el registro completo
 
Archivos asociados
Tamaño: 1.226Mb
Formato: PDF
.
Solicitar
Licencia
info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/141693
URL: https://linkinghub.elsevier.com/retrieve/pii/S0923181120301961
DOI: http://dx.doi.org/10.1016/j.jdermsci.2020.05.012
Colecciones
Articulos(IDEHU)
Articulos de INST.DE EST.DE LA INMUNIDAD HUMORAL PROF.R.A.MARGNI
Citación
Pinheiro Souza Neto, Fernando; Marinello, Poliana Camila; Melo, Gabriela Pasqual; Zambeli Naira Ramalho, Leandra; Cela, Eliana M.; et al.; Metformin inhibits the inflammatory and oxidative stress response induced by skin UVB-irradiation and provides 4-hydroxy-2-nonenal and nitrotyrosine formation and p53 protein activation; Elsevier Ireland; Journal of Dermatological Science; 100; 2; 11-2020; 152-155
Compartir
Altmétricas
 

Enviar por e-mail
Separar cada destinatario (hasta 5) con punto y coma.
  • Facebook
  • X Conicet Digital
  • Instagram
  • YouTube
  • Sound Cloud
  • LinkedIn

Los contenidos del CONICET están licenciados bajo Creative Commons Reconocimiento 2.5 Argentina License

https://www.conicet.gov.ar/ - CONICET

Inicio

Explorar

  • Autores
  • Disciplinas
  • Comunidades

Estadísticas

Novedades

  • Noticias
  • Boletines

Ayuda

Acerca de

  • CONICET Digital
  • Equipo
  • Red Federal

Contacto

Godoy Cruz 2290 (C1425FQB) CABA – República Argentina – Tel: +5411 4899-5400 repositorio@conicet.gov.ar
TÉRMINOS Y CONDICIONES