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Pamela Ferrari,Mariana Migliorini Parisi,Rafael Colombo,Matheus Becker,Gabriel Fries,Bruna Maria Ascoli,Luiza Paul Géa,Márcia Kauer-Sant’anna,Flávio Kapczinski,Fábio Klamt,Fátima T.C.R. Guma,Adriane R 대한정신약물학회 2018 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.16 No.1
Objective: Evidence has suggested that immune imbalance is involved with bipolar disorder (BD); however, its precise mechanism is poorly understood. This study investigated whether biochemical changes in the serum from BD patients could modulate the phenotype of cultured macrophages. Methods: Eighteen subjects with BD and five healthy individuals were included in this study. The human monocyte cell line U-937 was activated with phorbol 12-myristate 13-acetate (PMA) and polarization was induced with RPMI-1640 media supplemented with 10% serum from each patient for 24 hours. Gene expression of selected M1 and M2 markers was assessed by quantitative PCR. Results: Macrophages exposed to serum of manic and depressive BD patients displayed an increase of interleukin-1 (6.40±3.47 and 9.04±5.84 vs. 0.23±0.11; p<0.05) and tumor necrosis factor- (2.23±0.91 and 2.03±0.45 vs. 0.62±0.24; p=0.002 and p=0.004, respectively) compared to euthymic group (there was no difference between euthymic and controls). In parallel, U-937 macrophages treated with serum of patients in acute episode displayed a down-regulation of CXCL9 (0.29±0.20 vs. 1.86±1.61; p=0.006) and CXCL10 expression (0.36±0.15 and 0.86±0.24 vs. 1.83±0.88; p<0.000 and p=0.04) compared to the euthymia group. Conclusion: Our results are consistent with previous studies showing that changes in peripheral blood markers could modulate M1/M2 polarization in BD. The evidence of macrophages as source of inflammatory cytokines might be helpful to unravel how the mononuclear phagocyte system is involved in the etiology of BD.
Vitamin A Supplementation for Different Periods Alters Oxidative Parameters in Lungs of Rats
Matheus Augusto de Bittencourt Pasquali,Daniel Pens Gelain,Marcos Roberto de Oliveira,Guilherme Antônio Behr,Leonardo Lisbôa da Motta,Ricardo Fagundes da Rocha,Fábio Klamt,José Cláudio Fonseca Moreira 한국식품영양과학회 2009 Journal of medicinal food Vol.12 No.6
Lungs require an adequate supply of vitamin A (retinol) for normal embryonic development, postnatal maturation, and maintenance and repair during adult life. However, recent intervention studies revealed that supplementation with retinoids resulted in higher incidence of lung cancer, although the mechanisms underlying this effect are still unknown. Here, we studied the effect of vitamin A supplementation on oxidative stress parameters in lungs of Wistar rats. Vitamin A supplementation at either therapeutic (1,000 and 2,500IU/kg) or excessive (4,500 and 9,000IU/kg) doses for 3, 7, or 28 days induced lipid peroxidation, protein carbonylation, and oxidation of protein thiol groups, as well as change in catalase and superoxide dismutase activity. Together, these results suggest that vitamin A supplementation causes significant changes in redox balance, which are frequently associated with severe lung dysfunction.