Your browser doesn't support javascript.
loading
Metformin inhibits advanced glycation end products (AGEs)-induced renal tubular cell injury by suppressing reactive oxygen species generation via reducing receptor for AGEs (RAGE) expression.
Ishibashi, Y; Matsui, T; Takeuchi, M; Yamagishi, S.
Afiliación
  • Ishibashi Y; Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume, Japan.
Horm Metab Res ; 44(12): 891-5, 2012 Nov.
Article en En | MEDLINE | ID: mdl-22864903
Advanced glycation end products (AGEs) and their receptor (RAGE) play a role in tubulointerstitial damage in diabetic nephropathy. Recently, metformin has been shown to ameliorate tubular injury both in cell culture and diabetic animal model. However, effects of metformin on AGEs-induced tubular cell apoptosis and damage remain unknown. We examined here whether and how metformin could block the AGEs-RAGE-elicited tubular cell injury in vitro. Gene expression level was evaluated by real-time reverse-transcription polymerase chain reactions. Reactive oxygen species (ROS) generation was measured with dihydroethidium staining. Apoptosis was evaluated by DNA fragmentation and annexin V expression level. AGEs upregulated RAGE mRNA levels and subsequently increased ROS generation and intercellular adhesion molecule-1, monocyte chemoattractant protein-1 and transforming growth factor-ß gene expression in human renal proximal tubular cells, all of which were significantly blocked by the treatment of 0.01 and 0.1 mM metformin. Compound C, an inhibitor of AMP-activated protein kinase significantly blocked the effects of metformin on RAGE gene expression and ROS generation in AGEs-exposed tubular cells. Furthermore, metformin dose-dependently inhibited the AGEs-induced apoptotic cell death of tubular cells; 1 mM metformin completely suppressed the pro-apoptotic effects of AGEs in 2 different assay systems. Our present study suggests that metformin could inhibit the AGEs-induced apoptosis and inflammatory and fibrotic reactions in tubular cells probably by reducing ROS generation via suppression of RAGE expression through AMP-activated protein kinase activation. Metformin may protect against tubular cell injury in diabetic nephropathy by blocking the AGEs-RAGE-ROS axis.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores Inmunológicos / Regulación hacia Arriba / Especies Reactivas de Oxígeno / Productos Finales de Glicación Avanzada / Hipoglucemiantes / Túbulos Renales Proximales / Metformina Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Horm Metab Res Año: 2012 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Alemania

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores Inmunológicos / Regulación hacia Arriba / Especies Reactivas de Oxígeno / Productos Finales de Glicación Avanzada / Hipoglucemiantes / Túbulos Renales Proximales / Metformina Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Horm Metab Res Año: 2012 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Alemania