Flavonoids are a family of polyphenolic compounds which are widespread in nature (vegetables) and are consumed as part of the human diet in significant amounts. There are other types of polyphenols, including, for example, tannins and resveratrol. Flavonoids and related polyphenolic compounds have significant antiinflammatory activity, among others. This short review summarizes the current knowledge on the effects of flavonoids and related polyphenolic compounds on inflammation, with a focus on structural requirements, the mechanisms involved, and pharmacokinetic considerations. Different molecular (cyclooxygenase, lipoxygenase) and cellular targets (macrophages, lymphocytes, epithelial cells, endothelium) have been identified. In addition, many flavonoids display significant antioxidant/radical scavenging properties. There is substantial structural variation in these compounds, which is bound to have an impact on their biological profile, and specifically on their effects on inflammatory conditions. However, in general terms there is substantial consistency in the effects of these compounds despite considerable structural variations. The mechanisms have been studied mainly in myeloid cells, where the predominant effect is an inhibition of NF-κB signaling and the downregulation of the expression of proinflammatory markers. At present there is a gap in knowledge of in vitro and in vivo effects, although the pharmacokinetics of flavonoids has advanced considerably in the last decade. Many flavonoids have been studied for their intestinal antiinflammatory activity which is only logical, since the gastrointestinal tract is naturally exposed to them. However, their potential therapeutic application in inflammation is not restricted to this organ and extends to other sites and conditions, including arthritis, asthma, encephalomyelitis, and atherosclerosis, among others.
Intestinal mucosal barrier function is the capacity of the intestine to provide adequate containment of luminal microorganisms and molecules while preserving the ability to absorb nutrients. The central element is the epithelial layer, which physically separates the lumen and the internal milieu and is in charge of vectorial transport of ions, nutrients, and other substances. The secretion of mucus-forming mucins, sIgA, and antimicrobial peptides reinforces the mucosal barrier on the extraepithelial side, while a variety of immune cells contributes to mucosal defense in the inner side. Thus, the mucosal barrier is of physical, biochemical, and immune nature. In addition, the microbiota may be viewed as part of this system because of the mutual influence occurring between the host and the luminal microorganisms. Alteration of the mucosal barrier function with accompanying increased permeability and/or bacterial translocation has been linked with a variety of conditions, including inflammatory bowel disease. Genetic and environmental factors may converge to evoke a defective function of the barrier, which in turn may lead to overt inflammation of the intestine as a result of an exacerbated immune reaction toward the microbiota. According to this hypothesis, inflammatory bowel disease may be both precipitated and treated by either stimulation or downregulation of the different elements of the mucosal barrier, with the outcome depending on timing, the cell type affected, and other factors. In this review, we cover briefly the elements of the barrier and their involvement in functional defects and the resulting phenotype.
Background:Abdominal obesity is associated with coronary risk, although causality is not well established. Objective: In an obese Mediterranean population, we measured the fatty acid composition of adipose tissue, its relation with dietary fatty acids and central fat deposition, and its influence on plasma lipids and insulin. Design: Adipose tissue samples were obtained from 84 obese patients (29 men, 55 women) aged 30-70 y (body mass index, in kg/m 2 : 27-35). We measured concentrations of insulin and lipids in plasma and fatty acids in subcutaneous, omental, and perivisceral fat. Dietary fatty acid intake was assessed with a 7-d diet record. Results: The population studied was normolipidemic and normoinsulinemic. There were important differences in fatty acid composition between tissue sites: saturated fatty acids were higher and monounsaturated fatty acids were lower in perivisceral than in subcutaneous fat (P < 0.05). Significant correlations were found for oleic, linoleic, ␣-linolenic, and total nϪ6 polyunsaturated fatty acids between the subject's habitual diet and adipose tissue composition. Oleic and nϪ3 fatty acids from adipose regions were negatively correlated with apolipoprotein B and triacylglycerols; adipose tissue 22:1nϪ9, 20:2nϪ6, stearic acid, and eicosapentaenoic acid were positively correlated with HDL and apolipoprotein A; and adipose tissue myristic acid was negatively correlated with apolipoprotein A (P < 0.05). Central obesity was positively associated with nϪ6 polyunsaturated fatty acids and inversely associated with monounsaturated fatty acids and nϪ3 polyunsaturated fatty acids in adipose tissue (P < 0.05). Conclusion: The differences found in the composition and metabolism of perivisceral, omental, and subcutaneous fats may indicate that their atherogenic capacities also differ.Am J Clin Nutr 2001;74:585-91.
It is currently a routine practice to require a measurement of a housekeeping reference, including actin, glyceraldehyde-3-phosphate dehydrogenase, β-tubulin, among others, in Western blots, as it is the rule in RNA blots. Reversible Ponceau staining has been applied successfully to check equal loading of gels. Here we test a new technique, with the Stain-Free gels from Bio-Rad, against both Ponceau staining and housekeeping protein immunodetection under different conditions. Our results show that Stain-Free gels outperform Ponceau staining and that both are more consistent than housekeeping proteins as a loading control.
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