Effects of glutamine on the nuclear factor-kappaB signaling pathway of murine peritoneal macrophages |
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Authors: | Marcelo Macedo Rogero Primavera Borelli Ricardo Ambrósio Fock Maria Carolina Borges Marco Aurélio Ramirez Vinolo Rui Curi Karina Nakajima Amanda Rabello Crisma Aline Domingas Ramos Julio Tirapegui |
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Affiliation: | 1. Department of Nutrition, School of Public Health, S?o Paulo University, Avenida Doutor Arnaldo, 715, S?o Paulo, SP, 01246-904, Brazil 2. Department of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences, S?o Paulo University, 05508-900, S?o Paulo, SP, Brazil 3. Department of Physiology and Biophysics, Institute of Biomedical Sciences, S?o Paulo University, 05508-900, S?o Paulo, SP, Brazil 4. Department of Food and Experimental Nutrition, Faculty of Pharmaceutical Sciences, S?o Paulo University, 05508-900, S?o Paulo, SP, Brazil
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Abstract: | The aim of this study was to evaluate the effect of glutamine on the expression of proteins involved in the nuclear factor-kappaB (NF-κB) signaling pathway of murine peritoneal macrophages. Since glutamine is essential for the normal functioning of macrophages, it was hypothesized that in vitro glutamine supplementation would increase NF-κB activation. Peritoneal macrophages were pretreated with glutamine (0, 0.6, 2 and 10 mM) before incubation with lipopolysaccharide (LPS), and the effects of glutamine on the production of tumor necrosis factor-alpha and on the expression and activity of proteins involved in the NF-κB signaling pathway were studied by an enzyme linked immuno-sorbent assay, Western blotting, and an electrophoretic mobility shift assay. Glutamine treatment (2 and 10 mM) increased the activation of NF-κB in LPS-stimulated peritoneal macrophages (P < 0.05). In non-stimulated cells, glutamine treatment (2 and 10 mM) significantly reduced IκB-α protein expression (P < 0.05). Glutamine modulates NF-κB signaling pathway by reducing the level of IκB-α, leading to an increase in NF-κB within the nucleus in peritoneal macrophages. |
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