ASPECTOS GERAIS E ABORDAGEM TERAPÊUTICA DA QUERCETINA SOBRE AS COMPLICAÇÕES DO DIABETES CAUSADAS PELO ESTRESSE OXIDATIVO

Os flavonides pertencem classe de compostos fenlicos, que diferem entre si pela sua estrutura qumica e caractersticas particulares. Frutas, vegetais, gros, flores, ch e vinho so exemplos de fontes destes compostos. A quercetina o principal flavonide presente na dieta humana, sendo a representante mais caracterstica da subclasse flavonol da famlia dos flavonides. Desde a sua descoberta, os estudos publicados na literatura cientfica apontam para o seu papel crucial no combate ao estresse oxidativo, associado a diversas condies patolgicas. No diabetes mellitus (DM), por exemplo, tambm tem sido relatada sua eficincia na inibio da enzima aldose redutase que participa da via dos poliis. Nesta contextualizao e considerando as graves consequncias advindas do DM para a sade e qualidade de vida, props-se neste trabalho uma reviso geral da literatura pertinente, a fim de reunir dados sobre aspectos biolgicos e funcionais da quercetina, bem como, sua atuao benfica nas complicaes do diabetes causadas pelo estresse oxidativo

Restoration of density of interstitial cells of Cajal in the jejunum of diabetic rats after quercetin supplementation

Background: Interstitial cells of Cajal (ICC) are required for normal motility in the gastrointestinal tract. Depletion of ICC has been associated with diabetic gastroenteropathy. Aim: To determine the effect of quercertin supplementation on anoctamin-1 (Ano1) immunoreactive ICC in the myenteric region (ICC-MY) and deep muscular plexus (ICC-DMP) in the jejunum of diabetic rats. Methods: Thirty-two 90-day-old male Wistar rats were distributed into the following groups: normoglycemic (C), normoglycemic supplemented with quercetin (CQ; 40 mg daily), diabetic (D), and diabetic supplemented with quercetin (DQ; 40 mg daily). Diabetes was induced by streptozotocin injection. After 120 days, preparations of the jejunal muscular and submucosal layers were immunostained for Ano1 to visualize ICC. Evaluation of the immunofluorescence intensity as well as density of ICC was performed. Results: The density of ICC-MY was 46% lower in group D compared to group C (p 0.05). After quercertin treatment, the densities of ICC-MY were significantly higher in the DQ group compared to group D (ICC-MY: 58%, p 0.05). Conclusions: In STZ-treated diabetic rats, diabetes promoted a reduction in the density of jejunal ICC-MY with no significant effect on ICC-DMP. Supplementation with quercetin (DQ) appeared to protect ICC-MY from depletion in diabetes possibly due to its antioxidant action

Intestinal changes associated with fluoride exposure in rats: Integrative morphological, proteomic and microbiome analyses

Gastrointestinal signs and symptoms are the first signs of toxicity due to exposure to fluoride (F). This suggests the possibility that lower levels of subchronic F exposure may affect the gut. The aim of this study was to evaluate changes in the morphology, proteome and microbiome of the ileum of rats, after subchronic exposure to F. Male rats ingested water with 0, 10, or 50 mgF/L for thirty days. Treatment with F, regardless of the dose, significantly decreased the density of HuC/D-IR neurons, whereas CGRP-IR and SP-IR varicosities were significantly increased compared to the control group. Increased VIP-IR varicosities were significantly increased only in the group treated with 50 mgF/L. A significant increase in thickness of the tunica muscularis, as well as in the total thickness of the ileum wall was observed at both F doses when compared to controls. In proteomics analysis, myosin isoforms were increased, and Gastrotopin was decreased in F-exposed mice. In the microbiome metagenomics analysis, Class Clostridia was significantly reduced upon exposure to 10 mgF/L. At the higher F dose of 50 mg/L, genus Ureaplasma was significantly reduced in comparison with controls. Morphological and proteomics alterations induced by F were marked by changes associated with inflammation, and alterations in the gut microbiome. Further studies are needed to determine whether F exposure increases inflammation with secondary effects of the gut microbiome, and/or whether primary effects of F on the gut microbiome enhance changes associated with inflammation