Inhibition of Macrophage Oxidative Stress Prevents the Reduction of ABCA-1 Transporter Induced by Advanced Glycated Albumin
Carregando...
Citações na Scopus
25
Tipo de produção
article
Data de publicação
2012
Título da Revista
ISSN da Revista
Título do Volume
Editora
SPRINGER HEIDELBERG
Autores
PAIM, Bruno Alves
INADA, Natalia M.
VERCESI, Anibal Eugenio
Citação
LIPIDS, v.47, n.5, p.443-450, 2012
Resumo
We investigated the role of aminoguanidine and benfotiamine on the inhibition of reactive oxygen species (ROS) generation in macrophages induced by advanced glycated albumin (AGE-albumin) and its relationship with cell cholesterol homeostasis, emphasizing the expression of the ATP binding cassette transporter A-1 (ABCA-1). AGE-albumin was made by incubating fatty acid-free albumin with 10 mM glycolaldehyde. ROS production and ABCA-1 protein level were determined by flow cytometry in J774 macrophages treated along time with control (C) or AGE-albumin alone or in the presence of aminoguanidine or benfotiamine. Mitochondrial function was evaluated by oxygraphy. Compared to C-albumin, AGE-albumin increased ROS production in macrophages, which was ascribed to the activities of NADPH oxidase and of the mitochondrial system. Mitochondrial respiratory chain activity was reduced in cells incubated with AGE-albumin. ROS generation along time was associated with the reduction in macrophage ABCA-1 protein level. Aminoguanidine prevented ROS elevation and restored the ABCA-1 content in macrophages; on the other hand, benfotiamine that promoted a lesser reduction in ROS generation was not able to restore ABCA-1 levels. Inhibition of oxidative stress induced by AGE-albumin prevents disturbances in reverse cholesterol transport by curbing the reduction of ABCA-1 elicited by advanced glycation in macrophages and therefore may contribute to the prevention of atherosclerosis in diabetes mellitus.
Palavras-chave
Advanced glycation end products, ABCA-1, Oxidative stress, Aminoguanidine, Benfotiamine
Referências
- Basta G, 2005, ARTERIOSCL THROM VAS, V25, P1401, DOI 10.1161/01.ATV.0000167522.48370.5e
- Beisswenger PJ, 2001, DIABETES CARE, V24, P726, DOI 10.2337/diacare.24.4.726
- Brownlee M, 2001, NATURE, V414, P813, DOI 10.1038/414813a
- Cadenas E, 2000, FREE RADICAL BIO MED, V29, P222, DOI 10.1016/S0891-5849(00)00317-8
- Calcutt NA, 2009, NAT REV DRUG DISCOV, V8, P417, DOI 10.1038/nrd2476
- Castilho G, 2009, ATHEROSCLEROSIS, V10, pP713
- Fernyhough P, 2003, J PERIPHER NERV SYST, V8, P227, DOI 10.1111/j.1085-9489.2003.03028.x
- GLOMB MA, 1995, J BIOL CHEM, V270, P10017
- Hammes HP, 2003, NAT MED, V9, P294, DOI 10.1038/nm834
- Isoda K, 2007, ATHEROSCLEROSIS, V192, P298, DOI 10.1016/j.atherosclerosis.2006.07.023
- Iwashima Y, 2000, BIOCHEM BIOPH RES CO, V277, P368, DOI 10.1006/bbrc.2000.3685
- Kilhovd BK, 2007, DIABETOLOGIA, V50, P1409, DOI 10.1007/s00125-007-0687-z
- Kowaltowski AJ, 2009, FREE RADICAL BIO MED, V47, P333, DOI 10.1016/j.freeradbiomed.2009.05.004
- Machado AP, 2006, INT J BIOCHEM CELL B, V38, P392, DOI 10.1016/j.biocel.2005.09.016
- Machado-Lima A, 2009, ATHEROSCLEROSIS, V10, pP1133
- Mukherjee TK, 2005, BBA-MOL CELL RES, V1744, P213, DOI 10.1016/j.bbamcr.2005.03.007
- Nishikawa T, 2000, NATURE, V404, P787
- Oram JF, 2006, CIRC RES, V99, P1031, DOI 10.1161/01.RES.0000250171.54048.5c
- Passarelli M, 2005, DIABETES, V54, P2198, DOI 10.2337/diabetes.54.7.2198
- Schupp N, 2005, ANN NY ACAD SCI, V1043, P685, DOI 10.1196/annals.1333.079
- Wautier MP, 2001, AM J PHYSIOL-ENDOC M, V280, P685
- Wautier MP, 2001, AM J PHYSIOL-ENDOC M, V280, pE685
- WellsKnecht KJ, 1996, NEPHROL DIAL TRANSPL, V11, P41
- Yamagishi SI, 2011, BIOCH BIOPH IN PRESS