Resveratrol is an molecule that provides both anti-inflammatory and antioxidant properties. However, it is unclear whether the basal oxidative state of the cell has any influence on the effects of this compound. In humans, a single nucleotide polymorphism (SNP) is present in the enzyme manganese superoxide dismutase (SOD2), localized in codon 16 (rs4880), which can either be an alanine (A) or valine (V). This SNP causes an imbalance in the cellular levels of SOD2, where AA- and VV-genotypes result in higher or lower enzymatic activity, respectively. Furthermore, the VV-genotype has been associated with high levels of inflammatory cytokines. Here, we examined the effects of a range of resveratrol concentrations on the in vitro activation of human peripheral blood mononuclear cells (PBMCs) carrying different Ala16Val-SOD2 genotypes. Cell proliferation, several oxidative biomarkers and cytokines (IL-1β, IL-6, TNFα, Igγ and IL-10) were analyzed. In addition, the effects of resveratrol on the expression of the sirt1 gene were evaluated by qRT-PCR. After 24 h exposure to resveratrol, A-genotype PBMCs displayed a decrease in cell proliferation, whilst VV-cells contrasted; At 10 µM resveratrol, there was a significant decrease in the production of inflammatory cytokines in A-allele cells; however, VV-cells generally displayed a subtle decrease in these, except for TNFα, which was not affected. In all SOD2 genotypes cells exposed to resveratrol resulted in an upregulation of Sirt1 levels. Together, these results suggest that the effect of resveratrol on human PBMC activation is not universal and is dependent on the Ala16Val-SOD2 SNP.
Objective. This study aimed to test the effectiveness of copaiba, andiroba and aroeira essential oils for controlling trypanosomosis by Trypanosoma evansi with mice as experimental model. Materials and methods. Sixty-six mice were divided into eleven groups (A to L) with six animals each. Group A was the unique composed by healthy and uninfected animals (negative control). Animals in groups B to L were inoculated with 0.1 mL of blood containing 2.7 x 106 trypanosomes. Group B was used as a positive control without treatment. In experiment were tested copaiba (C, D and E), andiroba (F, G and H) and aroeira (I, J and L) oils at doses of 0.6, 0.8 and 1.0 mL kg-1 to infected mice (T. evansi). Results. These protocols did not provide curative efficacy; however, the mice treated with highest dose of copaiba showed a significant increase in the longevity when compared others groups. Conclusions. Previously in our studies, these essential oils have shown trypanocidal activity in vitro, but when they were tested in vivo in mice infected with T. evansi, this trypanocidal activity, or the curative effect was not found, being only able to prolong the lifespan of the animals treated with copaiba oil.
Li (lithium), a mood stabilizer has anti-inflammatory effect. However, in clinical practice, Li can be administered together with other antidepressants drugs, such as FLX (fluoxetine), IMI (imipramine), NOR (nortriptyline) and ESC (escitalopram). As interaction between Li and these antidepressant drugs on inflammatory modulation has not been investigated yet, we performed an in vitro protocol using a non-human macrophage cell line. Oxidative and inflammatory markers, as well as cell cycle analysis and cytokine gene expressions were compared among treatments. An IR (inflammatory ratio) was calculated based on the following oxidative-inflammatory variables: nitric oxide, superoxide anion, reactive oxygen molecules, cytokines IL-1β, IL-6, TNF-α and IL-10. The in vitro calculated IR data were validated through an in vivo analysis of 154 human subjects with similar IR. Li and control cells presented similar IR values. FLX, NOR and IMI increased slightly IR values indicating some proinflammatory effect, whereas ESC decreased IR values indicating some anti-inflammatory effect. However, cells exposed to Li + ESC triggered a proinflammatory response on macrophages. Thus, IR comparison results suggest that the Li anti-inflammatory effect is not universal and could be influenced by both basal macrophage-inflammatory state and interaction of other psychiatric drugs. These results could be useful to understand some inconsistencies observed in human studies involving Li and other psychiatric drugs.
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