Nutrimiromics studies the influence of the diet on the modification of gene expression due to epigenetic processes related to microRNAs (miRNAs), which may affect the risk for the development of chronic diseases. miRNAs are a class of non-coding endogenous RNA molecules that are usually involved in post-transcriptional gene silencing by inducing mRNA degradation or translational repression by binding to a target messenger RNA. They can be controlled by environmental and dietary factors, particularly by isolated nutrients or bioactive compounds, indicating that diet manipulation may hold promise as a therapeutic approach in modulating the risk of chronic diseases. This review summarizes the evidence regarding the influence of nutrients and bioactive compounds on the expression of miRNAs related to inflammation and chronic disease in several models (cell culture, animal models, and human trials).
Skeletal muscle protein turnover is modulated by intracellular signaling pathways involved in protein synthesis, degradation, and inflammation. The proinflammatory status of muscle cells, observed in pathological conditions such as cancer, aging, and sepsis, can directly modulate protein translation initiation and muscle proteolysis, contributing to negative protein turnover. In this context, branched-chain amino acids (BCAAs), especially leucine, have been described as a strong nutritional stimulus able to enhance protein translation initiation and attenuate proteolysis. Furthermore, under inflammatory conditions, BCAA can be transaminated to glutamate in order to increase glutamine synthesis, which is a substrate highly consumed by inflammatory cells such as macrophages. The present paper describes the role of inflammation on muscle remodeling and the possible metabolic and cellular effects of BCAA supplementation in the modulation of inflammatory status of skeletal muscle and the consequences on protein synthesis and degradation.
Moderate paper-filtered coffee consumption may have an undesirable effect on plasma cholesterol and inflammation biomarkers in healthy individuals regardless of its antioxidant content.
PM suppressed cell cycle progression mainly of HPC. This occurred via cyclin D1 down-regulation and p21/p27 overexpression attesting that BM microenvironment commitment observed in PM is affecting cell interactions compromising cell proliferation.
The objective of this study was to correlate the free radical scavenging and antioxidant activity of two known substances (Trolox and alpha-tocopherol), using three in vitro methods (linoleic acid emulsion, brain homogenate and 2,2-diphenyl-1-picryl-hydrazyl [DPPH]). At steady state, alpha-tocopherol showed a greater inhibition of spontaneous oxidation of brain homogenate (59.42%+/-1.91) than Trolox (38.50%+/-2.38), while the latter showed a better antioxidant activity performance regarding inhibition of linoleic acid peroxidation (100% versus 84.02%+/-1.98) and free radical scavenging activity (93.56%+/-5.71 versus 66.72%+/-6.28). When the IC50 value was used as a parameter, alpha-tocopherol presented greater antioxidant activity than Trolox evaluated in brain homogenate and DPPH, without a significant difference when using linoleic acid emulsion. Both compounds showed the same antioxidant efficiency measured by DPPH kinetics (0.37 mM). Antioxidant activity significantly changed according to the substrate, the parameter adopted to compare the substances in the same method and the form used to express antioxidant concentration.
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