| Autor: |
Aguilar EC; Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais/UFMG, Caixa Postal 486, 30161-970 Belo Horizonte, Brazil. edenilaguilar@gmail.com., Fernandes-Braga W; Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais/UFMG, Caixa Postal 486, 30161-970 Belo Horizonte, Brazil. edenilaguilar@gmail.com.; Precision Immunology Institute at the Icahn School of Medicine at Mount Sinai, New York, USA., Leocádio PCL; Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais/UFMG, Caixa Postal 486, 30161-970 Belo Horizonte, Brazil. edenilaguilar@gmail.com., Campos GP; Department of Pharmacology, Federal University of Minas Gerais, Belo Horizonte, Brazil. giannepcampos@gmail.com., Lemos VS; Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Brazil. vslemos@icb.ufmg.br., de Oliveira RP; Colégio Militar de Curitiba, Paraná, Brazil. raf_pires@hotmail.com., Caetano de Faria AM; Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais/UFMG, Caixa Postal 486, 30161-970 Belo Horizonte, Brazil. edenilaguilar@gmail.com., Dos Santos Aggum Capettini L; Department of Pharmacology, Federal University of Minas Gerais, Belo Horizonte, Brazil. giannepcampos@gmail.com., Alvarez-Leite JI; Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais/UFMG, Caixa Postal 486, 30161-970 Belo Horizonte, Brazil. edenilaguilar@gmail.com. |
| Abstrakt: |
Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disorder in the world. We have seen that gluten intake exacerbated obesity and atherosclerosis in apolipoprotein E knockout (ApoE-/-) mice. In this study, we investigated the effect of gluten consumption on inflammation and oxidative stress in the liver of mice with NAFLD. Male ApoE-/- mice were fed a gluten-free (GF-HFD) or gluten-containing (G-HFD) high-fat diet for 10 weeks. Blood, liver, and spleen were collected to perform the analyses. The animals of the gluten group had increased hepatic steatosis, followed by increased serum AST and ALT. Gluten intake increased hepatic infiltration of neutrophils, macrophages, and eosinophils, as well as the levels of chemotaxis-related factors CCL2, Cxcl2 , and Cxcr3 . The production of the TNF, IL-1β, IFNγ, and IL-4 cytokines in the liver was also increased by gluten intake. Furthermore, gluten exacerbated the hepatic lipid peroxidation and nitrotyrosine deposition, which were associated with increased production of ROS and nitric oxide. These effects were related to increased expression of NADPH oxidase and iNOS, as well as decreased activity of superoxide dismutase and catalase enzymes. There was an increased hepatic expression of the NF-κB and AP1 transcription factors, corroborating the worsening effect of gluten on inflammation and oxidative stress. Finally, we found an increased frequency of CD4+FOXP3+ lymphocytes in the spleen and increased gene expression of Foxp3 in the livers of the G-HFD group. In conclusion, dietary gluten aggravates NAFLD, exacerbating hepatic inflammation and oxidative stress in obese ApoE-deficient mice. |
